Amazon is accelerating and widening consumer refund payouts tied to a $2.5 billion settlement with the Federal Trade Commission, expanding eligibility for millions of additional customers who could now receive payments of up to $200 each.

The refunds stem from a historic settlement reached in September 2025, in which Amazon agreed to pay up to $1.5 billion in redress to consumers the FTC said were harmed by the company’s deceptive Prime enrollment and cancellation practices, in addition to a separate $1 billion civil penalty. As of September 2026, Amazon has issued more than $845 million in redress payments to affected consumers under that settlement.

Under an expanded federal court order, the eligibility criteria for those refunds is now broadening considerably. Previously focused on low-use Prime subscribers, the program will now also include millions of customers who used between 11 and 20 Prime benefits over a one-year period, a significantly larger pool of subscribers than the settlement initially targeted. Alongside that expanded eligibility, the maximum individual payment amount is increasing sharply, jumping from a previous cap of $51 to as much as $200 total per eligible consumer.

Consumers who have already received and cashed earlier refund checks under the original settlement terms are not being left out of the expanded program. Those individuals could receive an additional, automatic supplemental payment of up to $149, with that second round of payments expected to begin rolling out by April 2027.

Christopher Mufarrige, director of the FTC’s Bureau of Consumer Protection, framed the expanded order as a direct effort to ensure the settlement’s benefits reach a broader share of affected customers. “The revised order will ensure more consumers who were harmed by Amazon’s deceptive enrollment and cancellation practices benefit from the FTC’s historic settlement,” Mufarrige said.

The new round of payments is designed to require no action from eligible consumers. All new payments will be distributed automatically starting October 1, 2026, through PayPal, Venmo or a mailed paper check, depending on the payment information the FTC has on file or is able to obtain for each eligible consumer. Customers do not need to file any claims, complete any forms, or take any other proactive steps to receive their payment if they qualify under the expanded criteria.

That automatic, no-claim structure has also created an opening for potential fraud, prompting the FTC to issue a direct warning to consumers. The agency said anyone who contacts a consumer claiming to represent the FTC and asks for money, personal information or banking details in order to “claim” a refund is very likely running a scam. Because legitimate payments under the settlement are issued automatically without any request for personal or financial information, the FTC has emphasized that consumers should be highly skeptical of any unsolicited outreach asking them to take action, provide sensitive information, or pay a fee in order to receive a payment connected to the Amazon settlement.

The underlying case traces back to FTC allegations that Amazon made it deceptively easy for consumers to sign up for Prime subscriptions while making the cancellation process unreasonably difficult, a pattern regulators said resulted in many consumers being charged for a service they did not intend to continue using or, in some cases, did not realize they had signed up for in the first place. The $2.5 billion total settlement, combining the $1.5 billion consumer redress fund with the $1 billion civil penalty, ranked among the largest consumer protection settlements in FTC history when it was first announced in September 2025.

The expansion of eligibility criteria and the increase in maximum payment amounts reflect an acknowledgment by regulators that the original settlement terms may not have adequately captured the full scope of consumers affected by Amazon’s enrollment and cancellation practices. By extending eligibility to consumers who used a moderate number of Prime benefits, rather than limiting redress strictly to the lowest-use subscribers, the revised order is expected to bring a considerably larger share of Amazon’s Prime customer base within reach of some form of compensation under the settlement.

For consumers wondering whether they qualify for either the newly expanded initial payment or the supplemental payment tied to previously cashed checks, no application process exists, meaning eligible individuals should expect to be contacted or to simply receive payment directly through the channels described in the settlement, PayPal, Venmo, or a mailed check, without needing to search for or submit any documentation on their own behalf.

With payments set to begin rolling out automatically starting next month and the supplemental round for earlier claimants following by April 2027, the expanded settlement is expected to continue delivering compensation to Amazon Prime subscribers well into next year, as the FTC works through the process of identifying and distributing funds to the full population of consumers now covered under the revised order.

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Stanford University researchers have successfully transplanted lab-grown human brain tissue into genetically engineered mice, creating a new experimental platform scientists say could dramatically expand their ability to study neurological and psychiatric disorders that have long been difficult to research directly in living human brains.

The findings, published online September 16 in the journal Nature, describe an approach the research team calls “xenocortication.” Scientists engineered a strain of mice so that most of their neocortex and hippocampus, the brain regions responsible for higher cognitive functions and memory, never formed during early development. Researchers then transplanted human cortical organoids, self-organizing, three-dimensional clusters of laboratory-grown tissue that resemble specific regions of the developing brain, into the resulting cavity shortly after birth.

Cortical organoids are created by reprogramming human skin cells into induced pluripotent stem cells, which can then be coaxed to differentiate into most of the body’s cell types, including the specialized neurons and support cells found in the brain’s outer cortex. The technique builds on years of prior work by the study’s senior author, Sergiu Pașca, a neuroscientist and stem cell biologist who holds the Kenneth T. Norris Endowed Professorship in Psychiatry and Behavioral Sciences at Stanford and directs the university’s Brain Organogenesis Program.

According to Stanford’s own reporting on the study, the transplanted human tissue did not simply survive inside the mice; it expanded rapidly, eventually accounting for more than 90% of the total cortical tissue volume within the mice’s brains roughly three months after the transplant procedure. The human-derived neurons formed working connections both within the graft itself and with the surrounding mouse nervous system, with axons extending as far as the cervical spinal cord. Researchers also recorded coordinated electrical activity across the transplanted tissue, indicating the human cells were forming functional, organized circuits rather than simply existing as inert tissue.

Pașca described the significance of that integration directly. “In these mice, the human grafts generated a broad diversity of cortical cell types and established functional connections throughout the mouse nervous system,” he said. He was careful to characterize the limits of what the model represents, distinguishing it clearly from popular conceptions of “mini brains” grown in a dish. “They are not miniature brains and do not reproduce the full complexity of the human brain, but they allow us to study human neural cell types and developmental processes that would otherwise be extremely difficult to access,” Pașca said.

Remarkably, researchers found that the transplanted tissue contained detectable numbers of von Economo neurons, a rare and unusual type of nerve cell that had previously only been observed in postmortem human brain tissue and had never before been successfully generated either in laboratory culture or in earlier transplant experiments. Compared with previous cortical organoid transplant approaches, the xenocortical grafts also produced roughly three times more of a specific class of projection neurons that extend connections far beyond their region of origin, a feature researchers say makes the model considerably more representative of actual human cortical development than prior techniques.

Despite the scale of human tissue integration, the engineered mice retained largely normal function. Researchers found that so-called “apallial” mice, those genetically modified to lack most of their neocortex and hippocampus before any transplant occurred, were still able to move around their environment, see, hear and smell. Following the human tissue transplant, xenocortical mice performed on behavioral tests in a manner generally comparable to same-age normal mice by three to six months after surgery, despite carrying a brain composed overwhelmingly of human-derived cortical tissue.

To demonstrate the model’s potential research applications, scientists exposed xenocortical mice to five hours of low-oxygen conditions, designed to mimic aspects of the kind of oxygen deprivation that can occur around birth in human infants. That exposure caused substantial damage to the human-derived cortical tissue specifically, and oxygen-deprived xenocortical mice subsequently showed difficulty maintaining a steady gait and balance, a pattern researchers noted bears resemblance to symptoms seen in children with cerebral palsy. Normal mice and apallial mice lacking the human tissue transplant, by contrast, were largely unaffected by the same low-oxygen exposure. Pașca said understanding that difference could prove scientifically valuable well beyond the immediate experiment. “Finding out what accounts for this difference could yield clues about human neural susceptibility to oxygen deprivation, shed light on mechanisms underlying cerebral palsy and provide a platform for testing potential therapeutic strategies,” he said.

Researchers say the broader platform could eventually help scientists study a range of conditions that have historically been extremely difficult to investigate at the cellular and molecular level in living human brain tissue, including profound autism, schizophrenia, cerebral palsy and epilepsy. Alison Singer, president of the Autism Science Foundation, described the potential significance of the approach for future precision medicine efforts. “The idea that you can make an organoid model with an individual’s unique genetic character and use that to learn what’s gone awry in that individual’s brain is a critical step toward precision medicine,” Singer said.

Given the ethical complexity inherent in transplanting human neural tissue into animal models, Pașca organized a conference in Asilomar, California, in November 2025 specifically to debate the ethical implications of this kind of research before the study’s publication. Stanford’s Office of Technology Licensing holds patents related to the generation of cortical organoids, with Pașca listed as an inventor, along with a separate provisional patent application covering the organoid transplantation technique itself.

Researchers say the xenocortical mouse platform will primarily serve as a tool for studying how disease-associated genetic changes alter human neural development and circuit formation, and for testing whether potential treatments can prevent or reverse those changes, offering scientists a living system in which to study human brain biology that was previously accessible only through limited postmortem tissue samples or simplified laboratory cell cultures.