Steven Pete was born in 1981 in the 2,200-person town of Castle Rock, Washington, near Mount Saint Helens. At around 6 months old, when Pete started teething, he chewed off part of his tongue. As he got older he would bang his head against walls, not even stopping when it became swollen or indented. His parents made him wear a helmet, and they wrapped his arms and legs in long socks, securing them with duct tape, to prevent him from chewing away at his own limbs. His younger brother, Chris, had many of the same symptoms and all the same fearlessness. A day rarely passed when one of them didn’t bleed or bruise.

When his parents took Pete to a local pediatrician, they explained that they did not think he felt any pain. Maybe neither son did. The pediatrician hadn’t heard of a condition that prevented someone from experiencing pain, but after weeks of research, he found over 40 similar cases, including four siblings in Birmingham, England. The Pete boys were eventually diagnosed with congenital insensitivity to pain, and though the condition was likely passed down from one generation to another, there was no known cause, much less a cure.

Pete went on to live what appeared to be an ordinary life. In 2003, while working a security job at a mall, Pete met Jessica online. “We talked on the phone for hours,” Jessica remembers. Pete told her about his painlessness, and at the time she didn’t think much of it. “I guess I was like, ‘That’s pretty cool,’ ” she says now with a shrug. They married in 2005, and he started working at the Cowlitz Indian Tribe Health and Human Services Department. All that time, he was unaware that just a few hundred miles north, outside Vancouver, British Columbia, a small company was inching toward a breakthrough in understanding his condition.

For years that company, which is now called Xenon Pharmaceuticals, had been working to understand rare single-gene disorders such as familial exudative vitreoretinopathy (which causes vision loss) in order to create drugs that could be used to treat more common disorders with similar symptoms (like other conditions involving vision loss). In 2001 the company heard about a family in Newfoundland in which four members could not feel pain. One of the sons “actually stood on a nail and it had gone through his foot,” says Robin Sherrington, then senior director of biological sciences at Xenon. “He had no idea that it had happened until he got home and his parents saw it.” No gene had yet been linked with their condition, but given the familial links in the Newfoundland case, Xenon researchers suspected it was genetic. They started hunting for more subjects.

Following news reports and word of mouth, Xenon tracked down and studied 12 families from around the world with insensitivity to pain. (The Petes were not among them. Outside their immediate community, few people knew about the brothers’ condition.) For Sherrington, it was incredible that these individuals and their genomes existed. Evolution should have weeded out most of their ancestors. “Feeling pain is protective,” Sherrington says. “They would not have felt certain noxious stimuli. They should not have survived.” By studying those 12 families’ genomes throughout 2001 and 2002, Xenon found a common trait among those with insensitivity to pain: mutations in a single gene, SCN9A, and the non­functioning sodium channel it encodes, Nav1.7.

“This single channel, when it is nonfunctioning in a human being, renders them unable to understand or feel any form of pain,” Sherrington says, summarizing the team’s initial findings. And if Xenon could develop a new drug that could somehow mimic this condition—“to inhibit the Nav1.7 channel to partially replicate that absence of pain,” he explains—then it could relieve people’s pain without any of the side effects of opioids.

It is rare for biology to deliver such a seamless positive-negative effect within a single gene. In man on fire patients, one SCN9A mutation leads to a hyperactive Nav1.7 channel, which causes extreme discomfort. In those with insensitivity to pain, another SCN9A mutation leads to an inactive Nav1.7 channel, which results in total numbness. Given that the teams at Xenon and Yale were working on opposite coasts, and on conditions that fell on opposite sides of the pain spectrum, they only learned of each other’s discoveries through published reports and journal articles. (Sherrington first learned about Waxman’s study at Yale in 2004; Waxman only read about Sherrington’s work at Xenon after the company published its results in 2007.) Both teams arrived at the same clinical destination from a totally different direction, surprised as anyone that people like Pam Costa and Steven Pete had anything in common. “I was overwhelmed when we saw both sides of the genetic coin,” Waxman remembers. “SCN9A really is a master gene for pain.”

An interesting read via Wired News