Buckle up, cowboys.

Editor’s note: This blog, originally published on October 28, 2024, has been updated. Financial losses from worldwide credit card transaction fraud are projected to reach more than $403 billion over the next decade. The new NVIDIA AI Blueprint for financial fraud detection can help combat this burgeoning epidemic — using accelerated data processing and advanced algorithms to improve AI’s ability to detect and prevent credit card transaction fraud. Launched this week at the Money20/20 financial services conference, the blueprint provides a reference example for financial institutions to identify subtle patterns and anomalies in transaction data based on user behavior to improve accuracy and reduce false positives compared with traditional methods. It shows developers how to build a financial fraud detection workflow by providing reference code, deployment tools and a reference architecture. Companies can streamline the migration of their fraud detection workflows from traditional compute to accelerated compute using the NVIDIA AI Enterprise software platform and NVIDIA accelerated computing. The NVIDIA AI Blueprint is available for customers to run on Amazon Web Services, with availability coming soon on Dell Technologies and Hewlett Packard Enterprise. Customers can also use the blueprint through service offerings from NVIDIA partners including Cloudera, EXL, Infosys and SHI International. Businesses embracing comprehensive machine learning (ML) tools and strategies can observe up to an estimated 40% improvement in fraud detection accuracy, boosting their ability to identify and stop fraudsters faster and mitigate harm. As such, leading financial organizations like American Express and Capital One have been using AI to build proprietary solutions that mitigate fraud and enhance customer protection. The new AI Blueprint accelerates model training and inference, and demonstrates how these components can be wrapped into a single, easy-to-use software offering, powered by NVIDIA AI. Currently optimized for credit card transaction fraud, the blueprint could be adapted for use cases such as new account fraud, account takeover and money laundering. Using Accelerated Computing and Graph Neural Networks for Fraud Detection Traditional data science pipelines lack the compute acceleration to handle the massive data volumes required for effective fraud detection. ML models like XGBoost are effective for detecting anomalies in individual transactions but fall short when fraud involves complex networks of linked accounts and devices. Helping address these gaps, NVIDIA RAPIDS — part of the NVIDIA CUDA-X collection of microservices, libraries, tools and technologies — enables payment companies to speed up data processing and transform raw data into powerful features at scale. These companies can fuel their AI models and integrate them with graph neural networks (GNNs) to uncover hidden, large-scale fraud patterns by analyzing relationships across different transactions, users and devices. The use of gradient-boosted decision trees — a type of ML algorithm — tapping into libraries such as XGBoost, has long been the standard for fraud detection. The new AI Blueprint for financial fraud detection enhances the XGBoost ML model with NVIDIA CUDA-X Data Science libraries including GNNs to generate embeddings that can be used as additional features to help reduce false positives. The GNN embeddings are fed into XGBoost to create and train a model that can then be orchestrated. In addition, NVIDIA Dynamo-Triton, formerly NVIDIA Triton Inference Server, boosts real-time inferencing while optimizing AI model throughput, latency and utilization. NVIDIA CUDA-X Data Science and Dynamo-Triton are included with NVIDIA AI Enterprise. Leading Financial Services Organizations Adopt AI During a time when many large North American financial institutions are reporting online or mobile fraud losses continue to increase, AI is helping to combat this trend. American Express, which began using AI to fight fraud in 2010, leverages fraud detection algorithms to monitor all customer transactions globally in real time, generating fraud decisions in just milliseconds. Using a combination of advanced algorithms, one of which tapped into the NVIDIA AI platform, American Express enhanced model accuracy, advancing the company’s ability to better fight fraud. European digital bank bunq uses generative AI and large language models to help detect fraud and money laundering. Its AI-powered transaction-monitoring system achieved nearly 100x faster model training speeds with NVIDIA accelerated computing. BNY announced in March 2024 that it became the first major bank to deploy an NVIDIA DGX SuperPOD with DGX H100 systems, which will help build solutions that support fraud detection and other use cases. And now, systems integrators, software vendors and cloud service providers can integrate the new NVIDIA blueprint for fraud detection to boost their financial services applications and help keep customers’ money, identities and digital accounts safe. Explore the NVIDIA AI Blueprint for financial fraud detection and read this NVIDIA Technical Blog on supercharging fraud detection with GNNs. Learn more about AI for fraud detection by visiting the AI Summit at Money20/20, running this week in Amsterdam. See notice regarding software product information.

Version 1.0.0 By Robert Jan van Pelt (Park Books, 2025) The largest artifact in the touring exhibition Auschwitz. Not Long Ago. Not Far Away., currently on display at the ROM in Toronto, is a wooden barracks building. It’s from the Auschwitz-Monowitz camp, a satellite to Auschwitz created to provide slave labour to the IG Farben corporation for the construction of a synthetic rubber factory.  The discovery of a sister building, back in 2012, led exhibition chief curator and architectural historian Robert Jan van Pelt, University Professor at the Waterloo School of Architecture, on a research journey to write a comprehensive history of the barracks—temporary buildings that have not only housed prisoners, but also provided shelter for military servicemen and women, refugees, and natural disaster survivors. “Many people have experienced, for shorter or longer time periods, life in a barrack, and for all of them it represented life on the edge, for better or worse,” writes Van Pelt. Worm’s eye axonometric of Renkioi Hospital Barrack, a prefabricated hospital designed by Ismabard Kingdom Brunel for a site in Turkey, 1857. Van Pelt’s book criss-crosses with ease through architectural history, military history, and the history of medicine—all of which played crucial roles in the evolving development of this seemingly simple building type. The book is arranged in a dozen episodes, with the barrack at the centre of each, serving as an anchor point for unfolding the rich intellectual and historical context shaping the way these structures were developed and deployed. The book is richly illustrated with archival materials—a feat in itself, given that the documentation for temporary buildings, particularly before 1900, is scarce. These drawings, photos, and paintings are supplemented with 20 worm’s eye views of key buildings, carefully composed by a team of Waterloo architecture school students and alumni.  Thomas Thomaszoon, View of the headquarters of the Spanish in the Huis tea Kleef during the siege of Haarlem, 1572-73. Collection of Noord-Hollands Archief, Haarlem; courtesy Robert Jan van Pelt Like many vernacular buildings, temporary structures larger than a tent, designed to house soldiers in the field, have existed at least since Ancient Rome. One of the first visual accounts of barracks came centuries later, in the winter of 1572, when the Spanish laid siege to the Dutch city of Haarlem, and cartographer Thomas Thomaszoon sketched the position of dozens of Spain’s wood-and-straw structures outside the city. The siege was successful, but only a few years later, the Dutch Republic gained the upper hand. As part of the creation of a standing army, they began to develop more precise instructions for the layout of camps, including the construction of temporary barracks. Antoine-François Omet des Foucaux, Barrack constructed in Hendaye, France, 1793. From Jean-Charles Krafft, Plans, coupes et élévations de diverses productions de l’art de la charpente, 1805. Collection of Bilbliothèque Nationale de France, Paris. Courtesy Robert Jan van Pelt The Napoleonic army made use of barracks in both military camps and training camps; by the mid-1800s, the construction of various barrack types was detailed in field construction manuals issued to officers in many European armies. During the Crimean War (1853-56), over 3,500 prefabricated barracks were manufactured in a Gloucester factory, as a solution to the appalling conditions at the front. But when the structures arrived at port, British forces were not able to unload and erect them—the materials for a single building weighed more than two tons, and each would require 60 horses (or 150 men) to transport to camp on the muddy roads.  The US (Union) Army’s Lincoln Hospital, Washington, DC, 1865. Collection of Library of Congress, Washington, DC. Courtesy Robert Jan van Pelt Prefabrication was also used, with somewhat more success, towards the end of the conflict to erect field hospitals designed by British engineer Isambard Kingdom Brunel with a priority on cross-ventilation to limit the spread of disease. Low mortality rates from similar structures led to a continued preference for “barrack hospitals” based on groupings of low-slung, well-ventilated pavilions, rather than conceived as single grand structures. The model was further refined with the addition of primitive underfloor heating and ridge ventilation by former surgeon William A. Hammond for the Union Army during the American Civil War (1861-65).  Barrack hospitals were constructed for civilian use, as well. Following the conclusion of the Franco-Prussian war (1870-71), such designs were built to house patients with infectious diseases in Berlin and proposed as a means to bring professional medical care to Germany’s rural areas. A barracks-inspired hospital was built in Saint Petersburg, Russia, in 1889, and continues to be operational.  If the barrack as an accommodation for the sick is a progressive tale, the 19th-century history of the barrack is equally checkered by the building type’s use for prisoner accommodation, including in the penal colonies of Australia and French Guiana. In North America, barracks were used in an internment camp for Native American Dakotas, and Civil War-era Union barracks at Camp Douglas were used to house Confederate prisoners. The oldest preserved barrack in the world may be in Canada, at Grosse Isle national park. Here, barrack-style quarantine sheds were used to detain thousands of Irish immigrant families during the typhoid fever epidemic of 1846-47, and their damp, fetid conditions contributed to many deaths—an episode Van Pelt describes as a “blot on the national consciousness of Canada.” A single Doecker Hut contains an operation room, pharmacy and hospital management office. The prefabricated, portable hospitals were developed in 1885, and used around the world, including in the First World War. In America, they were marketed for managing epidemics in the wake of the 1892 typhus fever outbreak in New York. Courtesy Berlin State Library and Robert Jan van Pelt   At the turn of the 19th century, the prefabricated portable barrack came to the fore with the manufacturing of the Doecker barracks, by Christoph & Unmack, a firm based in Copenhagen and Germany. Developed by a former military officer-turned-tentmaker, the technically sophisticated model used large rectangular frames that could be clipped together, and covered with “felt-cardboard”—dense felt pressed onto canvas and impregnated with linseed oil. The self-supporting structures proved easy to set up, dismount, and transport, making them suitable for both military applications—and, with little modification, for humanitarian aid. The Red Cross deployed Doecker barracks for use as field hospitals in Manchuria and Yokohama during the Russo-Japanese War (1904-05).  The Barrack, 1572-1914 wraps up in in the early 20th century, but with the note that in the ensuing decades until 1945, millions of barracks were produced by many of the world’s major nations—and that most of these were erected in barbed-wire-ringed compounds. “This is the period in which tens if not hundreds of millions of people, many of whom were civilians, were forced to live in barracks, as refugees, as expellees, as civilian internees, as forced laborers, as prisoners or war, as concentration camp prisoners, and as people made homeless by the destruction wrought by war,” writes Van Pelt. Up until 1914, he notes, this building type largely carried a sense of achievement—an image that would change sharply with the Age of the Camps. But although a WWII barrack was responsible for instigating Van Pelt’s initial investigation, that time period will need to await a second volume on this simple building type with a rich, complex, and complicated history.   As appeared in the June 2025 issue of Canadian Architect magazine  The post Book Review: The Barrack, 1572-1914—Chapters in the History of Emergency Architecture appeared first on Canadian Architect.

Why it matters: It's somewhat ironic that arguably the biggest piracy enabler today is a device that comes from Amazon, a $2 trillion tech giant with a streaming service. According to a new report, jailbroken Amazon Fire Sticks are used to watch billions of dollars worth of pirated streams, and Google, Meta and Microsoft are exacerbating the situation. A report from Enders Analysis, titled "Video piracy: Big tech is clearly unwilling to address the problem," looks at the issue of illegal streams. Driving the piracy epidemic, particularly in Europe, is the sports broadcasting industry. The BBC reports that the overall value of media rights for this business passed $60 billion last year, which means fans are paying increasingly higher prices to watch sports on TV, especially if they pay for multiple services. UK soccer fans had to pay around $1,171 in the 23/24 season if they wanted to watch all televised Premier League games. The same is also true for mainstream streamers such as Netflix and Disney Plus, which keep raising their subscription costs and clamping down on account sharing. Paying so much in these economically uncertain times has pushed more people into canceling their legitimate streaming services and turning to pirated alternatives. The report notes that Tom Burrows, head of global rights at the world's largest European soccer streamer, DAZN, called streaming piracy "almost a crisis for the sports rights industry." // Related Stories Comcast-owned European TV giant Sky Group echoed the warnings. It said piracy was costing the company "hundreds of millions of dollars" in revenue. Many high-profile events, such as major games, can draw tens of thousands of viewers away from legal services and toward the many pirated streams showing the same content at a fraction of the price – or free. Most people are familiar with jailbroken Amazon Fire Sticks being used to access illegal streaming services – the report calls the device a "piracy enabler." According to Sky, 59% of people who watched pirated material in the UK over the last year did so using a Fire Stick. The report says that the device enables "billions of dollars in piracy" overall. Would you pirate this pirate show? "People think that because it's a legitimate brand, it must be OK. So they give their credit card details to criminal gangs. Amazon is not engaging with us as much as we'd like," said Sky Group COO Nick Herm. As with all forms of piracy, there are risks associated with this trend. Providing credit card details and email addresses to those behind the services isn't exactly safe, and there have been cases of jailbroken, malware-infested pirate streaming devices – not just Fire Sticks – being sold on eBay, Craigslist, and the dark web. There has been a crackdown on the sale of hacked Fire Sticks in the UK recently. Last year saw a man given a two-year suspended sentence for selling the devices, while another was jailed. Just using these sticks or illegal IPTV subscriptions is breaking the law. It's not just Amazon that is being blamed. The report highlights Facebook's lack of action to stop ads for illegal streams running on the platform. Google and Microsoft are also called out for the "continued deprecation" of their respective DRM systems, Widevine and PlayReady; the report says they "are now compromised across various security levels." Microsoft's last update to PlayReady was December 2022. "Over twenty years since launch, the DRM solutions provided by Google and Microsoft are in steep decline," reads the report. "A complete overhaul of the technology architecture, licensing, and support model is needed. Lack of engagement with content owners indicates this a low priority." Amazon says it is working with industry partners and relevant authorities to combat piracy and protect customers from the risks associated with pirated content. The company has taken (or is about to take) steps to make turning Fire TV-branded devices into piracy boxes more difficult. These include raising the technical bar (ADB over local network disabled, tighter DRM), and adding warning messages about legality. Moreover, Amazon is switching Fire TV devices from Android to the Linux-based Vega OS later this year, which doesn't run Android APKs at all.

Co-lead author Ravneet Sidhu examines an ancient human tooth at the McMaster Ancient DNA Centre. (Image Credit: McMaster University)NewsletterSign up for our email newsletter for the latest science newsA new study in Science suggests that changes in a gene in Yersinia pestis, the bacterium that causes plague, could’ve added to the length of two plague pandemics, including the pandemic that started with the “Black Death.” “Ours is one of the first research studies to directly examine changes in an ancient pathogen, one we still see today, in an attempt to understand what drives the virulence, persistence, and eventual extinction of pandemics,” said Hendrik Poinar, a study author and the director of the McMaster Ancient DNA Centre, according to a press release.The study suggests that less virulent plague bacteria could’ve caused longer plague pandemics — thanks to the fact that infected rodents lived (and spread plague) for longer periods of time before dying from their infections. Read More: Scientists Reveal the Black Death’s Origin StoryThe Three Plague PandemicsThe bacterium Y. pestis infects rodents and humans alike and has caused three main plague pandemics in humans, all of which continued for centuries after their initial outbreaks. The first began in the 500s; the second began in the 1300s; and the third started in the 1800s (and still continues in certain areas in Asia, Africa, and the Americas today). Although all three pandemics were devastating at their outset, the second pandemic was by far the most severe. The Black Death, its initial outburst, killed around 30 to 50 percent of the population of Europe between 1347 and 1352 and — to this day — represents the deadliest disease wave in recorded history.To learn more about how these plague pandemics changed over time, scientists at McMaster University in Canada and the Institut Pasteur in France turned to a Y. pestis virulence gene known as pla. This gene is repeated many times throughout the Y. pestis genome, and it allows the bacterium to spread undetected throughout the bodies of infected individuals. A Gene and the PlagueTo investigate this gene, the scientists studied historical strains of Y. pestis from human remains and found that the number of repetitions of pla decreased over the course of the first and second plague pandemics. Then, the scientists tested Y. pestis bacteria from the third pandemic, infecting mice with three strains that had reduced repetitions of pla. “These three samples enabled us to analyze the biological impact of these pla gene deletions,” said Javier Pizarro-Cerdá, another study author and the director of the Yersinia Research Unit at the Institut Pasteur, according to the release.The results revealed that pla depletion decreases the virulence and increases the length of plague infections in mice. According to the study authors, these changes could have caused rodents to live longer in the later stages of the first and second pandemics, allowing them to spread their infections for a longer period. “It’s important to remember that plague was an epidemic of rats, which were the drivers of epidemics and pandemics. Humans were accidental victims. ” Poinar added in another press release.The Continued Threat of Y. PestisThough the pla depletion occurred around 100 years after the first and second pandemics began, the scientists stress that both changes were random and unrelated.“Our research sheds light on an interesting pattern in the evolutionary history of the plague. However, it is important to note that the majority of strains which continue to circulate today in Africa, the Americas, and Asia are highly virulent strains,” said Ravneet Sidhu, another study author and a Ph.D. student at the McMaster Ancient DNA Centre.Though still a threat to current populations, Y. pestis infections are much more manageable now as a result of modern diagnostics and treatments.“Today, the plague is a rare disease, but one that remains a public health concern and serves as a model for gaining a broad understanding of how pandemics emerge and become extinct. This example illustrates the balance of virulence a pathogen can adopt in order to spread effectively,” Pizarro-Cerdá said in the press release.Article SourcesOur writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:Science. Sam Walters is a journalist covering archaeology, paleontology, ecology, and evolution for Discover, along with an assortment of other topics. Before joining the Discover team as an assistant editor in 2022, Sam studied journalism at Northwestern University in Evanston, Illinois.1 free article leftWant More? Get unlimited access for as low as $1.99/monthSubscribeAlready a subscriber?Register or Log In1 free articleSubscribeWant more?Keep reading for as low as $1.99!SubscribeAlready a subscriber?Register or Log In

A Fungal Disease Ravaged North American Bats. Now, Researchers Found a Second Species That Suggests It Could Happen Again White-nose syndrome caused millions of bat deaths, and scientists are sounding the alarm that a second fungus could be disastrous if it reaches American wildlife Lillian Ali - Staff Contributor May 30, 2025 A little brown bat (Myotis lucifugus) is seen with white fuzz on its nose, a characteristic of the deadly white-nose syndrome. Ryan von Linden / New York Department of Environmental Conservation In February 2006, a cave explorer near Albany, New York, took the first photograph of bats with a mysterious white growth on their faces. Later, biologists studying the mammals in caves and mines discovered piles of dead bats in the state—also with the fuzzy white mold. The scientists were floored. For years, no one knew what was causing the mass die-offs from this “white-nose syndrome.” In early 2007, Albany residents called local authorities with reports of typically nocturnal bats flying in broad daylight. “They were just dying on the landscape,” wildlife biologist Alan Hicks told the Associated Press’ Michael Hill in 2008. “They were crashing into snowbanks, crawling into woodpiles and dying.” At last, scientists identified a culprit: The bats had succumbed to an infection caused by the fungus Pseudogymnoascus destructans. Since its initial discovery, white-nose syndrome has killed millions of bats across 40 U.S. states and nine Canadian provinces, making it “the most dramatic wildlife mortality event that’s ever been documented from a pathogen,” DeeAnn Reeder, a disease ecologist at Bucknell University, tells the New York Times’ Carl Zimmer. Now, nearly two decades later, scientists have developed some promising ways to fend off the disease, including an experimental vaccine. But a new study published this week in the journal Nature warns of a newly discovered second species of fungus that, if it reaches North America, could set all that progress back. “We thought we knew our enemy, but we have now discovered it is twice the size and potentially more complex than we had imagined,” lead author Nicola Fischer, a biologist at the University of Greifswald in Germany, says in a statement. Little brown bats are susceptible to white-nose syndrome in North America. Krynak Tim, U.S. Fish and Wildlife Service The team analyzed 5,479 fungus samples collected by hundreds of citizen science volunteers across North America, Asia and Europe. They found that white-nose syndrome is caused by two distinct fungal species native to Europe and Asia, with only one species having reached North America so far. If the second species hits the continent, it could look like a “reboot” of the epidemic, Reeder tells the New York Times. Study co-author Sébastien Puechmaille, an evolutionary biologist at the University of Montpellier in France, knew bats in Europe had also been seen with white fuzz on their noses, as he tells the New York Times. But those populations didn’t die off like American bats. Charting the disease across Europe and Asia, he noticed that the fungus was able to live alongside those bats, while it ravaged American ones. In its native range, the fungus grows in the bodies of hibernating bats as their internal temperature drops, then it’s shed in the spring when they awaken. But in American bats, the fungus causes their immune systems to activate and burn fat reserves as they hibernate. The bats then wake up periodically, causing irregular activity and eventual starvation. The researchers suggest the damaging fungal spores were first brought to North America by cavers that traveled from Europe—potentially western Ukraine—to the United States without completely disinfecting their boots or rope. White-nose syndrome poses a threat not just to bats, but to whole ecosystems. Bats are vital parts of many food chains, eating insects and pollinating plants. However, they reproduce fairly slowly, only having one or two pups at a time. Rebuilding a bat population, then, could take decades. And since cave ecosystems are similarly delicate, biologists are wary of trying to kill off the fungus preemptively. “Cave ecosystems are so fragile that if you start pulling on this thread, what else are you going to unravel that may create bigger problems in the cave system?” said University of Wisconsin–Madison wildlife specialist David Drake to the Badger Herald’s Kiran Mistry in December. The discovery also occurs as the original wave of white-nose syndrome continues to spread across North America, having just crossed the Continental Divide in Colorado. Just one spore of the new species could be devastating to American bat colonies. Puechmaille tells the New York Times that policies should be put in place to make sure the second fungus does not spread to more continents, and that cavers should not move equipment between countries and should disinfect it regularly. “This work … powerfully illustrates the profound impact a single translocation event can have on wildlife,” he adds in the statement. Get the latest stories in your inbox every weekday.

There are some questionable sources underpinning Robert F. Kennedy Jr.‘s controversial “Make America Healthy Again” commission report. Signs point to AI tomfoolery, and the use of ChatGPT specifically, which calls into question the veracity of the White House report meant to address reasons for the decline in US life expectancy.An investigation by NOTUS found dozens of errors in the MAHA report, including broken links, wrong issue numbers, and missing or incorrect authors. Some studies were misstated to back up the report’s conclusions, or more damningly, didn’t exist at all. At least seven of the cited sources were entirely fictitious, according to NOTUS.Another investigation by The Washington Post found that at least 37 of the 522 citations appeared multiple times throughout the report. Notably, the URLs of several references included “oaicite,” a marker that OpenAI applies to responses provided by artificial intelligence models like ChatGPT, which strongly suggests its use to develop the reportGenerative AI tools have a tendency to spit out false or incorrect information, known as “hallucinations.” That would certainly explain the various errors throughout the report — chatbots have been found responsible for similar citation issues in legal filings submitted by AI experts and even the companies building the models. Nevertheless, RFK Jr has long advocated for the “AI Revolution,” and announced during a House Committee meeting in May that “we are already using these new technologies to manage health care data more efficiently and securely.”In a briefing on Thursday, press secretary Karoline Leavitt responded to concerns about the accuracy of the citations while evading any mention of AI tools. Leavitt described the errors as “formatting issues” and defended the health report for being “backed on good science that has never been recognized by the federal government.” The Washington Post notes that the MAHA report file was updated on Thursday to remove some of the oaicite markers and replace some of the non-existent sources with alternative citations. In a statement given to the publication, Department of Health and Human Services spokesman Andrew Nixon said “minor citation and formatting errors have been corrected, but the substance of the MAHA report remains the same — a historic and transformative assessment by the federal government to understand the chronic disease epidemic afflicting our nation’s children.”See More:

Let’s start with one unambiguous fact: More children are diagnosed with autism today than in the early 1990s. According to a sweeping 2000 analysis by the Centers for Disease Control and Prevention, a range of 2–7 per 1,000, or roughly 0.5 percent of US children, were diagnosed with autism in the 1990s. That figure has risen to 1 in 35 kids, or roughly 3 percent.The apparent rapid increase caught the attention of people like Robert F. Kennedy Jr., who assumed that something had to be changing in the environment to drive it. In 2005, Kennedy, a lawyer and environmental activist at the time, authored an infamous essay in Rolling Stone that primarily placed the blame for the increased prevalence of autism on vaccines. (The article was retracted in 2011 as more studies debunked the vaccine-autism connection.) More recently, he has theorized that a mysterious toxin introduced in the late 1980s must be responsible. Now, as the nation’s top health official leading the Department of Health and Human Services, Kennedy has declared autism an “epidemic.” And, in April, he launched a massive federal effort to find the culprit for the rise in autism rates, calling for researchers to examine a range of suspects: chemicals, molds, vaccines, and perhaps even ultrasounds given to pregnant mothers. “Genes don’t cause epidemics. You need an environmental toxin,” Kennedy said in April when announcing his department’s new autism research project. He argued that too much money had been put into genetic research — “a dead end,” in his words — and his project would be a correction to focus on environmental causes. “That’s where we’re going to find an answer.”But according to many autism scientists I spoke to for this story, Kennedy is looking in exactly the wrong place. Three takeaways from this storyExperts say the increase in US autism rates is mostly explained by the expanding definitions of the condition, as well as more awareness and more screening for it.Scientists have identified hundreds of genes that are associated with autism, building a convincing case that genetics are the most important driver of autism’s development — not, as Health Secretary Robert F. Kennedy Jr. has argued, a single environmental toxin.Researchers fear Kennedy’s fixation on outside toxins could distract from genetic research that has facilitated the development of exciting new therapies that could help those with profound autism.Autism is a complex disorder with a range of manifestations that has long defied simple explanations, and it’s unlikely that we will ever identify a single “cause” of autism.But scientists have learned a lot in the past 50 years, including identifying some of the most important risk factors. They are not, as Kennedy suggests, out in our environment. They are written into our genetics. What appeared to be a massive increase in autism was actually a byproduct of better screening and more awareness. “The way the HHS secretary has been walking about his plans, his goals, he starts out with this basic assumption that nothing worthwhile has been done,” Helen Tager-Flusberg, a psychologist at Boston University who has worked with and studied children with autism for years, said. “Genes play a significant role. We know now that autism runs in families… There is no single underlying factor. Looking for that holy grail is not the best approach.”Doctors who treat children with autism often talk about how they wish they could provide easy answers to the families. The answers being uncovered through genetics research may not be simple per se, but they are answers supported by science.Kennedy is muddying the story, pledging to find a silver-bullet answer where likely none exists. It’s a false promise — one that could cause more anxiety and confusion for the very families Kennedy says he wants to help. Robert F. Kennedy Jr. speaks during a news conference at the Department of Health and Human Services in mid-April to discuss this agency’s efforts to determine the cause of autism. Alex Wong/Getty ImagesThe autism “epidemic” that wasn’tAutism was first described in 1911, and for many decades, researchers and clinicians confused the social challenges and language development difficulties common among those with the condition for a psychological issue. Some child therapists even blamed the condition on bad parenting. But in 1977, a study discovered that identical twins, who share all of their DNA, were much more likely to both be autistic than fraternal twins, who share no more DNA than ordinary siblings. It marked a major breakthrough in autism research, and pushed scientists to begin coalescing around a different theory: There was a biological factor.At the time, this was just a theory — scientists lacked the technology to prove those suspicions at the genetic level. And clinicians were also still trying to work out an even more fundamental question: What exactly was autism? For a long time, the criteria for diagnosing a person with autism was strictly based on speech development. But clinicians were increasingly observing children who could acquire basic language skills but still struggled with social communication — things like misunderstanding nonverbal cues or taking figurative language literally. Psychologists gradually broadened their definition of autism from a strict and narrow focus on language, culminating in a 2013 criteria that included a wide range of social and emotional symptoms with three subtypes — the autism spectrum disorder we’re familiar with today.Along the way, autism had evolved from a niche diagnosis for the severely impaired to something that encompassed far more children. It makes sense then, that as the broad criteria for autism expanded, more and more children would meet it, and autism rates would rise. That’s precisely what happened. And it means that the “epidemic” that Kennedy and other activists have been fixated on is mostly a diagnostic mirage. Historical autism data is spotty and subject to these same historical biases, but if you look at the prevalence of profound autism alone — those who need the highest levels of support — a clearer picture emerges. (There is an ongoing debate in the autism community about whether to use the terminology of “profound autism” or “high support needs” for those who have the most severe form of the condition.) In the ’80s and ’90s, low-support needs individuals would have been less likely to receive an autism diagnosis given the more restrictive criteria and less overall awareness of the disorder, meaning that people with severe autism likely represented most of the roughly 0.5 percent of children diagnosed with autism in the 1990s. (One large analysis from Atlanta examining data from 1996 found that 68 percent of kids ages 3 to 10 diagnosed with autism had an IQ below 70, the typical cutoff for intellectual disability.)By 2025, when about 3 percent of children are being diagnosed with autism, about one in four of those diagnosed are considered to have high-support needs autism, those with most severe manifestation of the condition. That would equal about 0.8 percent of all US children — which would be a fairly marginal increase from autism rates 30 years ago. Or look at it another way: In 2000, as many as 60 percent of the people being diagnosed with autism had an intellectual disability, one of the best indicators of high-support needs autism. In 2022, that percentage was less than 40 percent.As a recently published CDC report on autism prevalence among young children concluded, the increase in autism rates can largely be accounted for by stronger surveillance and more awareness among providers and parents, rather than a novel toxin or some other external factor driving an increase in cases.Other known risk factors — like more people now having babies later in their life, given that parental age is linked to a higher likelihood of autism — are more likely to be a factor than anything Kennedy is pointing at, experts say. “It’s very clear it’s not going to be one environmental toxin,” said Alison Singer, founder of the Autism Science Foundation and parent of a child with profound autism. “If there were a smoking gun, I think they would have found it.”While Kennedy has fixated on vaccines and environmental influences, scientists have gained more precision in mapping human genetics and identifying the biological mechanisms that appear to be a primary cause of autism. And that not only helps us understand why autism develops, but potentially puts long-elusive therapies within reach. It began with an accident in the 1990s. Steven Scherer, now director of the Center for Applied Genomics at the Hospital for Sick Children in Toronto, began his career in the late 1980s trying to identify the gene that caused cystic fibrosis — in collaboration with Francis Collins, who went on to lead the Human Genome Project that successfully sequenced all of the DNA in the human genome in the early 2000s. Scherer and Collins’s teams focused on chromosome 7, identified as a likely target by the primitive genetic research available at the time, a coincidence that would reorient Scherer’s career just a few years later, putting him on the trail of autism’s genetic roots.After four years, the researchers concluded that one gene within chromosome 7 caused cystic fibrosis. Soon after Scherer helped crack the code on cystic fibrosis in the mid-1990s, two parents from California called him: He was the world’s leading expert on chromosome 7, and recent tests had revealed that their children with autism had a problem within that particular chromosome.That very same week, Scherer says, he read the findings of a study by a group at Oxford University, which had looked at the chromosomes of families with two or more kids with autism. They, too, had identified problems within chromosome 7.“So I said, ‘Okay, we’re going to work on autism,’” Scherer told me. He helped coordinate a global research project, uniting his Canadian lab with the Oxford team and groups in the US to run a database that became the Autism Genome Project, still the world’s largest repository of genetic information of people with autism.They had a starting point — one chromosome — but a given chromosome contains hundreds of genes. And humans have, of course, 45 other chromosomes, any of which conceivably might play a role. So over the years, they collected DNA samples from thousands upon thousands of people with autism, sequenced their genes, and then searched for patterns. If the same gene is mutated or missing across a high percentage of autistic people, it goes on the list as potentially associated with the condition. Scientists discovered that autism has not one genetic factor, but many — further evidence that this is a condition of complex origin, in which multiple variables likely play a role in its development, rather than one caused by a single genetic error like sickle-cell anemia.Here is one way to think about how far we have come: Joseph Buxbaum, the director of the Seaver Autism Center for Research and Treatment at the Icahn School of Medicine at Mount Sinai in New York, entered autism genetics research 35 years ago. He recalls scientists being hopeful that they might identify a half dozen or so genes linked to autism.They have now found 500 genes — and Buxbaum told me he believed they might find a thousand before they are through. These genetic factors continue to prove their value in predicting the onset of autism: Scherer pointed to one recent study in which the researchers identified people who all shared a mutation in the SHANK3 gene, one of the first to be associated with autism, but who were otherwise unalike: They were not related and came from different demographic backgrounds. Nevertheless, they had all been diagnosed with autism.Researchers analyze the brain activity of a 14-year-old boy with autism as part of a University of California San Francisco study that involves intensive brain imaging of kids and their parents who have a rare chromosome disruption connected to autism. The study, the Simons Variation in Individuals Project, is a genetics-first approach to studying autism spectrum and related neurodevelopmental disorders. Michael Macor/San Francisco Chronicle via The Associated PressPrecisely how much genetics contributes to the development of autism remains the subject of ongoing study. By analyzing millions of children with autism and their parents for patterns in diagnoses, multiple studies have attributed about 80 percent of a person’s risk of developing autism to their inherited genetic factors. But of course 80 percent is not 100 percent. We don’t yet have the full picture of how or why autism develops. Among identical twins, for example, studies have found that in most cases, if one twin has high-support needs autism, the other does as well, affirming the genetic effect. But there are consistently a small minority of cases — 5 and 10 percent of twin pairs, Scherer told me — in which one twin has relatively low-support needs while the one requires a a high degree of support for their autism.Kennedy is not wholly incorrect to look at environmental factors — researchers theorize that autism may be the result of a complex interaction between a person’s genetics and something they experience in utero. Scientists in autism research are exploring the possible influence when, for example, a person’s mother develops maternal diabetes, high blood sugar that persists throughout pregnancy. And yet even if these other factors do play some role, the researchers I spoke to agree that genetics is, based on what we know now, far and away the most important driver.“We need to figure out how other types of genetics and also environmental factors affect autism’s development,” Scherer said. “There could be environmental changes…involved in some people, but it’s going to be based on their genetics and the pathways that lead them to be susceptible.”While the precise contours of Health Department’s new autism research project is still taking shape, Kennedy has that researchers at the National Institutes of Health will collect data from federal programs such as Medicare and Medicaid and somehow use that information to identify possible environmental exposures that lead to autism. He initially pledged results by September, a timeline that, as outside experts pointed out, may be too fast to allow for a thorough and thoughtful review of the research literature. Kennedy has since backed off on that deadline, promising some initial findings in the fall but with more to come next year.RFK Jr.’s autism commission research risks the accessibility of groundbreaking autism treatmentsIf Kennedy were serious about moving autism science forward, he would be talking more about genetics, not dismissing them. That’s because genetics is where all of the exciting drug development is currently happening.A biotech firm called Jaguar Gene Therapy has received FDA approval to conduct the first clinical trial of a gene therapy for autism, focused on SHANK3. The treatment, developed in part by one of Buxbaum’s colleagues, is a one-time injection that would replace a mutated or missing SHANK3 gene with a functional one. The hope is that the therapy would improve speech and other symptoms among people with high-needs autism who have also been diagnosed with a rare chromosomal deletion disorder called Phelan-McDermid syndrome; many people with this condition also have Autism spectrum disorder.The trial will begin this year with a few infant patients, 2 years old and younger, who have been diagnosed with autism. Jaguar eventually aims to test the therapy on adults over 18 with autism in the future. Patients are supposed to start enrolling this year in the trial, which is focused on first establishing the treatment’s safety; if it proves safe, another round of trials would start to rigorously evaluate its effectiveness.“This is the stuff that three or four years ago sounded like science fiction,” Singer said. “The conversation has really changed from Is this possible? to What are the best methods to do it? And that’s based on genetics.”Researchers at Mount Sinai have also experimented with delivering lithium to patients and seeing if it improves their SHANK3 function. Other gene therapies targeting other genes are in earlier stages of development. Some investigators are experimenting with CRISPR technology, the revolutionary new platform for gene editing, to target the problematic genes that correspond to the onset of autism.But these scientists fear that their work could be slowed by Kennedy’s insistence on hunting for environmental toxins, if federal dollars are instead shifted into his new project. They are already trying to subsist amid deep budget cuts across the many funding streams that support the institutions where they work. “Now we have this massive disruption where instead of doing really key experiments, people are worrying about paying their bills and laying off their staff and things,” Scherer said. “It’s horrible.” For the families of people with high-needs autism, Kennedy’s crusade has stirred conflicting emotions. Alison Singer, the leader of the Autism Science Foundation, is also the parent of a child with profound autism. When I spoke with her, I was struck by the bind that Kennedy’s rhetoric has put people like her and her family in. Singer told me profound autism has not received enough federal support in the past, as more emphasis was placed on individuals who have low support needs included in the expanding definitions of the disorder, and so she appreciates Kennedy giving voice to those families. She believes that he is sincerely empathetic toward their predicament and their feeling that the mainstream discussion about autism has for too long ignored their experiences in favor of patients with lower support needs. But she worries that his obsession with environmental factors will stymie the research that could yield breakthroughs for people like her child.“He feels for those families and genuinely wants to help them,” Singer said. “The problem is he is a data denier. You can’t be so entrenched in your beliefs that you can’t see the data right in front of you. That’s not science.”See More:

PlaySafe ID raises $1.12m in pre-seed funding round Digital identity platform to use funds in support of its "go-for-market" launch to safeguard gamers Image credit: PlaySafe ID News by Sophie McEvoy Staff Writer Published on May 30, 2025 PlaySafe ID has raised $1.12 million in a pre-seed funding round led by Early Game Ventures. With participation from Hartmann Capital and Overwolf, the funding will expand PlaySafe ID's digital identity platform as it prepares a "go-for-market" launch targeting 250,000 users. PlaySafe ID issues players with a "verified, anonymous, and game-agnostic digital ID" to prove that a user "is real and hasn't been caught cheating or being inappropriate to children". The firm is currently in talks "with several major gaming platforms" and is aiming to announce its first partnerships later this year. "This round gives us the firepower to move fast, expand our world-class team, and partner with games that want the most fair and safe environment for players to enjoy," said PlaySafe ID CEO Andrew Wailes. "With cheating in games as a mass epidemic that ruins fun for players daily, and the Online Safety Act ushering in long overdue requirements for child protection in gaming, PlaySafe ID's mission to safeguard gamers isn't just relevant – it's now essential for compliance and the future of global gaming." Early Game Ventures managing partner Cristian Munteanu added: "We believe PlaySafe ID is building the trust later for gaming – and beyond. "In a world where AI and anonymity are eroding safety and fairness, PlaySafe ID restores balance with identity, transparency, and accountability. Once a gamer is verified through PlaySafe ID, that identity becomes portable across games, platforms, and genres." Munteanu concluded: "The more developers adopt it, the more valuable it becomes to players – and vice versa. Eventually, the verified identity becomes a default layer of the gaming stack, just like your Steam account or your Xbox Live profile. It's a winner-takes-all kind of play."

The astounding drop in violent crime that began in the 1990s and extended through the mid-2010s is one of the most important — and most underappreciated — good news stories of recent memory. That made its reversal during the pandemic so worrying.In the first full year of the pandemic, the FBI tallied 22,134 murders nationwide, up from 16,669 in 2019 — an increase of roughly 34 percent, the sharpest one-year rise in modern crime record-keeping. In 2021, Philadelphia alone recorded a record 562 homicides, while Baltimore experienced a near-record 337 murders. Between 2019 and 2020, the average number of weekly emergency department visits for gunshots increased by 37 percent, and largely stayed high through the following year. By the 2024 election, for the first time in awhile, violent crime was a major political issue in the US. A Pew survey that year found that 58 percent of Americans believed crime should be a top priority for the president and Congress, up from 47 percent in 2021. And yet even as the presidential campaign was unfolding, the violent crime spike of the pandemic had already subsided — and crime rates have kept dropping. The FBI’s 2023 crime report found that murder was down nearly 12 percent year over year, and in 2024 it kept falling to roughly 16,700 murders, on par with pre-pandemic levels. The early numbers for 2025 are so promising that Jeff Asher, one of the best independent analysts on crime, recently asked in a piece whether this year could have the lowest murder rate in US history.All of which raises two questions: What’s driving a decrease in crime every bit as sharp as the pandemic-era increase? And why do so many of us find it so hard to believe?The crime wave crashesWe shouldn’t jump to conclusions about this year’s crime rates based on the early data, especially since we’re just now beginning the summer, when violent crime almost always rises. Crime data in the US is also patchy and slow — I can tell you how many soybeans the US raised in March, but I can’t tell you how many people have been murdered in the US this year. But what we can tell looks very good. The Real-Time Crime Index, an academic project that collects crime data from more than 380 police agencies covering nearly 100 million people, estimates there were 1,488 murders in the US this year through March, compared to an estimated 1,899 over the same months last year. That’s a decrease of nearly 22 percent. Violent crime overall is down by about 11 percent. Motor vehicle theft, which became an epidemic during the pandemic, is down by over 26 percent. Peer down to the local level, and the picture just keeps getting better. In Baltimore, which The Wire made synonymous with violent, drug-related crime, homicides fell to 199 last year, its best showing in over a decade. As of early May, the city had 45 murders, down another third from the same period last year. City emergency rooms that were once full of gunshot victims have gone quiet.How much lower could it go nationally? The record low homicide rate, at least since national records started being kept in 1960, is 4.45 per 100,000 in 2014. So far this year, according to Asher, murder is down in 25 of the 30 cities that reported the most murders in 2023. Asher argues that if the numbers hold, “a 10 percent or more decline in murder nationally in 2025 would roughly tie 2014 for the lowest murder rate ever recorded.”What’s behind the drop?In short: The pandemic led to a huge increase in violent crime, and as the pandemic waned, so did the wave.The closure of schools during the pandemic, especially in already higher-crime cities in the Northeast, meant far more young men — who are statistically more likely to be either perpetrators of violent crime or victims of it — on the streets. The closure of social services left fewer resources for them to draw on; and the sheer stress of a once-in-a-lifetime health catastrophe set everyone on edge. The murder of George Floyd in spring 2020 led to a collapse in community trust in policing, which in turn seemed to lead to less aggressive policing altogether. As the pandemic eased, though, those buffers came back, providing a natural brake on violent crime.But the government, from the national level down to cities, also took direct actions to stem the flood of violence. The White House under President Joe Biden poured hundreds of millions of dollars into community violence interruption programs, which aim to break the cycle of retribution that can lead to homicide. Baltimore’s Group Violence Reduction Strategy has brought together community groups and law enforcement to deter the people considered most likely to get involved in gun violence. And the erosion in police forces nationwide that occurred during the pandemic has largely stopped. The situation is far from perfect. Even though Floyd’s murder triggered a nationwide reckoning around police violence, recent data shows that police killings kept increasing, in part because fear of crime often stopped momentum around reforms. Here in New York, even as overall crime on the subways has fallen to historical lows, felony assaults on the trains have kept rising, fueling fears of lawlessness. Why can’t we believe it?As Memorial Day weekend marks the start of summer, the next few months will tell whether the pandemic was truly just a blip in the long-term reduction in violent crime. But what we can say is most people don’t seem to notice the positive trends. An October 2024 poll by Gallup found that 64 percent of Americans believed there was more crime nationwide than the year before, even though by that time in 2024, the post-pandemic crime drop was well under way. But such results aren’t surprising. One of the most reliable results in polling is that if you ask Americans whether crime is rising, they’ll say yes. Astonishingly, in 23 of 27 national surveys done by Gallup since 1993, Americans reported that they thought crime nationwide was rising — even though most of those surveys were done during the long crime decline. Crime is one of the best examples we have of bad news bias. By definition, a murder is an outlier event that grabs our attention, inevitably leading the nightly local news. Sometimes, as during the pandemic, that bias can match reality. But if we fail to adjust to what is actually happening around us — not just what we think is happening — it won’t just make us think our cities are more dangerous than they really are. It’ll sap energy for the reforms that can really make a difference. A version of this story originally appeared in the Good News newsletter. Sign up here!You’ve read 1 article in the last monthHere at Vox, we're unwavering in our commitment to covering the issues that matter most to you — threats to democracy, immigration, reproductive rights, the environment, and the rising polarization across this country.Our mission is to provide clear, accessible journalism that empowers you to stay informed and engaged in shaping our world. By becoming a Vox Member, you directly strengthen our ability to deliver in-depth, independent reporting that drives meaningful change.We rely on readers like you — join us.Swati SharmaVox Editor-in-ChiefSee More: