NewLimit—a startup spearheaded by Coinbase founder Brian Armstrong—is set to give the goal a shot. On Tuesday the company announced it had raised $40 million in a Series A round from Kleiner Perkins and other venture firms—and from prominent investors like former Google CEO Eric Schmidt and Y Combinator CEO Garry Tran, Fortune’s Jeff John Roberts reported.

Armstrong declined to make specific predictions about how many years the company’s research may extend life. Instead, he emphasized that its focus is on “healthspan” versus “lifespan”—a goal that centers on quality of life, not length.

“The mission at NewLimit is to radically extend human healthspan, which is intended to give us more healthy years,” Armstrong told Fortune. “I think it’s important to make that distinction.”

NewLimit is currently focused on making discoveries, not on developing products, Armstrong emphasized. He compared NewLimit to SpaceX, saying that Elon Musk’s 2002 landmark start-up aims to get to Mars eventually, but has managed to “get some satellites into orbit” in the meantime.

“And that actually helps them on their journey to get to Mars, because it helps them perfect the technology needed for the broader mission,” Armstrong said.

Just how exactly NewLimit plans to accomplish its war on aging is unknown. Here is some of what we do know, however, about aging and the science behind reversing it.

How are genetics involved in aging?

In short: It’s complicated. Longevity—or how long one lives—is the result of an interplay between genetics, the environment, and lifestyle, according to the NIH’s National Library of Medicine. 

About a quarter of the variation in human lifespan is likely attributable to genetics, though it’s unknown exactly which genes contributed to longevity, and exactly how they do. Variations on some genes associated with long human life—including APOE, FOXO3, and CETP—have been identified. But those variations aren’t present in all of those who have lived into their 80s, 90s, 100s, and beyond, meaning science still has its detective work cut out for it. What’s more, it’s possible that variations in genes act collectively to contribute to longevity, in ways science doesn’t fully understand.

How do epigenetics play a role in the aging process?

Exactly why each of us ages like we do—and why some age “better” than others—is still poorly understood. There is no one “key” to explain aging, including genetics. But epigenetics may hold a bulk of the answers, especially as to why some closely related individuals age so differently. 

Epigenetics is the study of the epigenome, which consists of chemicals that modify the genome, telling it “what to do, where to do it, and when to do it”—almost like computer software. It can be influenced, or “reprogrammed,” by environmental factors like stress, diet, drugs, and pollution. Resulting changes can be passed down from cell to cell as they divide, within an individual—and from generation to generation, among family members.

In the 1990s, researchers studied the aging of yeast cells and determined that epigenetic information was lost with time, causing cells to lose their identity. Thus, scientists turned to the epigenome as a potential cause of aging in living organisms in general. According to some theories, damage to the epigenome may be more responsible for aging than damage to DNA itself.

If chemicals can inadvertently modify the genome, researchers began to wonder, why can’t humans modify it on purpose, in a bid to reverse the harms of modern living?

Already, epigenetic reprogramming, via the modification of cells, has been proven to alleviate symptoms of aging and/or extend the lifespan in animals, according to a 2022 article in the journal Signal Transduction and Targeted Therapy. 

What’s more, a landmark 13-year study published in January found that the loss of epigenetic information in mice causes aging—and that the restoration of that information reverses signs of aging. The study’s Harvard-lead research team believes it to be the first to demonstrate that epigenetic changes are the primary cause of aging in mammals.

How does NewLimit plan to reverse aging?

The company’s website says it plans to use epigenetic reprogramming “to develop new medicines for age-related diseases.” It plans to use recent advances in single cell genomics, epigenetic editing, and machine learning “to overcome traditional roadblocks” to the process, it states.

The company will initially focus on T-cells—a type of white blood cell that helps protect the body from infection, and may fight cancer—geneticist Blake Byers, one of the company’s four co-founders, told Fortune’s Roberts.

Is there promise in epigenetic reprogramming?

The January-published Havard-lead study on epigenetic reprogramming in mice provides “long-awaited confirmation that DNA changes are not the only—or even the main—cause of aging,” according to the university. Because it’s easier to manipulate the epigenome than to reverse DNA mutations, epigenetic reprogramming could provide a more efficient—and effective—route to preventing or treating age-related disease.

The study was the first to show “that we can have precise control of the biological age of a complex animal, that we can drive it forwards and backwards at will,” the study’s lead researcher, David Sinclair, professor of genetics in the Blavatnik Institute at Harvard Medical School and co-director of the Paul F. Glenn Center for Biology of Aging Research, said in a news release at the time.

Results must be replicated in non-human primates, and studies are underway, researchers said, cautioning that medical applications are a long way off. But the end goal—of extending the human healthspan—holds promise and is worthy of pursuit, they contended.

“We’re talking about taking someone who’s old or sick and making their whole body or a specific organ young again, so the disease goes away,” Sinclair said at the time, referencing the study. “It’s a big idea. It’s not how we typically do medicine.”