On April 24, 2003, shortly after the completion of the human genome project, its director Francis Collins and his team posed 15 grand challenges to the scientific community. They dared researchers to harness the genome to crack puzzles of biology, health, and society. In particular, they called for genome-based tools to close health disparities. Since then, the United States has pumped more than $1 billion a year into genomics research. What do we have to show for it?

“What we found in the literature published from 2007 to 2013 was basically nothing,” said Jay Kaufman, the lead author of the first study to examine available genetic data for evidence that explains a major racial-health disparity. For many years, researchers speculated that what they couldn’t explain about disparities must be the fingerprint of some mysterious genetic component. But since they are now able to scan the entire genome, this speculation appears both lazy and wrong. When it comes to why many black people die earlier than white people in the U.S., Kaufman and his colleagues show we've been looking for answers in the wrong places: We shouldn't be looking in the twists of the double helix, but the grinding inequality of the environment.

It is no secret that a longer life is a white privilege in the U.S. In 2011, the Centers for Disease Control and Prevention (CDC) reported that white men lived more than four years longer than black men, and white women lived more than three years longer than black women. The main reason for the racial mortality gap is heart disease. “There’s a huge number of years of life lost because some people have the black life expectancy and not the white life expectancy,” Kaufman said. “It’s killing people prematurely on the basis of race.”

To understand if there is any genetic reason for these deaths, Kaufman’s team reviewed six years of genome-wide studies of cardiovascular disease. Having crawled across the genome for every possible variant that could trigger deadlier disease, they only found three that fit the bill—and two of them suggested that whites, not blacks, should be on the suffering side of the disparity. “We’re spending a huge amount of money on these studies,” he said, “but if you are interested in understanding disparities, all this money that’s been spent has come up with basically nothing.”

Maybe this finding isn’t entirely earth-shattering. After all, it is almost universally agreed that race is a social construct. In 2005, only two years after the sequencing of the human genome, the editors of Nature Biotechnology put it like this: “Pooling people in race silos is akin to zoologists grouping raccoons, tigers, and okapis on the basis that they are all stripey.” Perhaps, then, the better question is: Why do we continue to search for a connection between race and genetics to explain health disparities?

One reason has less to do with biology and more to do with finances. Take BiDil, the first race-specific medication, which made a cameo on House, M.D. BiDil is a combination of two generic drugs for heart failure that have been on the scene for decades. In 2005, the Food and Drug Administration approved the old drugs for a new purpose: the treatment of heart failure in a single race, African Americans. Jonathan Kahn, author of Race in a Bottle, has written extensively on the history of this medication. There is no doubt that BiDil works for African Americans. The sleight of hand, Kahn points out, is that the clinical trial for the drug’s approval—the African American Heart-Failure Trial—had no comparison group. Researchers only studied BiDil in African Americans. The drug likely worked not because they are black, but because they are human. But the juicier claim is that NitroMed, the company behind BiDil, was able to extend its patent to 2020, which otherwise would have expired in 2007. The magic touch was the race-specific label, which made the old method new again.

Another reason for the persistence of race and genetics in biomedical research is much more subtle. Certain diseases cluster in populations, such as Tay-Sachs, which is most common in people with an Ashkenazi Jewish background. In such cases, some researchers say we should turn our attention away from race and toward ancestry. If it is true that there are differences in disease risk between human groups, then what we need is a more clever way to dice up humanity. “It has nothing to do with race, it has more to do with ancestry,” explained Rick Kittles, the director of the Center for Population Genetics at the University of Arizona and co-founder of African Ancestry, Inc. “We talk about ancestry, we talk about shared genetic backgrounds. That is a better proxy for biology than race. If someone says they’re of Ashkenazi Jewish ancestry, and they have a family history of Tay-Sachs, that’s not because of a race. That’s because of shared ancestry. If a person of West African descent has a family history of prostate cancer, that’s a shared genetic background.”

But this only takes us in a circle. Even when researchers study ancestry, it is often just race in a phony moustache and glasses. Take the creation of ancestry informative markers (AIMs). They are a collection of genetic variants between four populations: Europeans, West Africans, Indigenous Americans, and East Asians. They are used for both the sort of recreational ancestry mapping that promises to uncover roots and to understand disease risk. In 2007, an article in Science magazine with 14 co-authors, including Kaufman, pointed out some of the problems with this model: People from the Middle East and India are classified as ‘Native American’, even though “no archaeological, genetic, or historical evidence supports this suggestion,” and East Africans are left out of the mix entirely.

Duana Fullwiley, an anthropologist at Stanford, took an even closer look at how AIMs were dreamed up and used in the laboratories of some prominent researchers—Mark Shriver at Penn State and Esteban González Burchard at UCSF. What she found is that this new system is no better than a find-and-replace of “race” with “ancestry.” In one striking example, she unearthed a patent application that straight-up defines biogeographical ancestry as simply “the heritable component of race.” In her 2008 article, “The Biologistical Construction of Race,” Fullwiley concludes that “the very continents and peoples chosen for this product were selected due to their perceived proximity to what we in North America imagine race to be.”

Even if scientists could get ancestry right, and pry it apart from society’s tightly held beliefs about race, it still wouldn’t account for enough disease to explain health disparities. “If you look at overall health disparities across the board,” Kittles said, “the bulk of those disparities are not due to any biological difference. The vast majority of health disparities are due to social, behavioral, and environmental components.”

Why hasn’t attention turned, then, to social inequality, not genetics, as the source of health disparities? The main reason is the political ramification. “If you show that this is a predisposition that is genetically determined—black people just have this gene, there’s nothing we can do about it, this is just nature—then society is completely absolved. We don’t have any responsibility to solve this problem,” Kaufman said. “If you show that it is because of racism and injustice and people’s living conditions, well, then, there is some responsibility and we have to do something about this.”

In his book Making the Mexican Diabetic: Race, Science, and Inequality, Michael Montoya shows how epidemiologists try to explain diabetes through genetics, even if evidence points in a social direction: lifestyle disruptions, dispossession, and poverty, which disproportionately affect minorities. “It is much easier to say it must be something [wrong] with those people than it is [to say something’s wrong] with the way we have arranged our society,” Montoya told me.

Even when doctors and policymakers try to address health disparities, and not simply phantom genetic differences, there tends to be too much focus on technology, drugs, and devices. The former surgeon general, David Satcher, and his colleagues say that this is a mistake. What’s needed, they say, is investment in equity and infrastructure.

As a thought experiment, say that scientists got ancestry right and cooked up a drug that closed the cardiovascular disease mortality gap. Would it do any good? Considering that more than half a million black residents on the south and west sides of Chicago live in pharmacy deserts, the answer isn’t so clear. “Even if you have a prescription from physician, do you have access to a pharmacy?” asked Dima Qato, the lead author of the breakthrough study on Chicago’s pharmacy deserts. What good is a silver-bullet drug without an equitable delivery system?

In Chicago, six of the seven neighborhoods that have the lowest life expectancy are segregated African-American neighborhoods. The neighborhoods with the highest life expectancy are less than 10 percent African-American. To look for the cause of this racial disparity in genetics isn’t only scientifically flawed. It is morally flawed as well.