People Who Cannot Feel Pain Exist — Their Genes Will End Chronic Pain for Millions by 2038

The Question

In the early 2000s, doctors in Pakistan encountered a teenage street performer who earned money by pushing knives through his arms and walking across burning coals, feeling nothing. He was not enduring the pain; he simply had none to endure. He and several relatives shared a rare inherited condition, and when geneticists traced its cause, they found a single broken gene. That gene, called SCN9A, builds a tiny protein channel — a molecular gate named Nav1.7 — that lets nerve cells fire the electrical signals we experience as pain. Without a working gate, the message never leaves the body's alarm system.

This condition, congenital insensitivity to pain, is dangerous for those who have it: they burn, break bones, and bite through their tongues without warning. But it handed medicine an extraordinary gift. It revealed, with certainty no drug trial could match, that pain in humans depends on one identifiable switch. The question now is whether scientists can build medicines that dial that switch down on demand — relieving suffering without turning it off forever, and crucially, without the addiction that makes today's strongest painkillers so destructive.

What the Evidence Shows

The genetic story is unusually clean. Loss-of-function mutations in SCN9A — where the gene is switched off — produce people who feel no pain. The mirror-image condition, called erythromelalgia, is caused by gain-of-function mutations in the same gene, where the channel is stuck too far open; those patients suffer episodes of burning agony in their hands and feet. Two opposite faults in one gene, producing no pain and unbearable pain, is about as strong as biological evidence gets. Related genes, including SCN11A and PRDM12, cause similar pain-free conditions, reinforcing the map of the body's pain machinery.

Drug companies have spent years racing to block these sodium channels safely, and the first real success has already arrived. In early 2025, the US Food and Drug Administration approved suzetrigine, marketed as Journavx and developed by Vertex Pharmaceuticals, for moderate-to-severe short-term pain. It works by blocking a closely related channel, Nav1.8, in the nerves outside the brain and spinal cord. It is the first genuinely new class of non-opioid painkiller approved in decades, and because it acts on peripheral nerves rather than the brain's reward circuits, it does not carry the addiction risk of opioids.

The stakes are enormous. Chronic pain affects roughly one in five adults, and for years the strongest relief on offer was opioids — effective but addictive, and at the centre of a crisis that has killed hundreds of thousands of people. A painkiller that matches opioids for strength without hooking the patient is one of medicine's most valuable prizes. Suzetrigine is the opening move; the deeper goal is to target Nav1.7 itself, the exact channel the pain-free families revealed, and eventually to reach chronic conditions rather than just short-term pain.

Why This Is Happening

The target is validated by human genetics, not just animal models. Most drugs fail because they work in mice but not in people. Here the proof came from human beings living without pain their entire lives. That certainty about the mechanism dramatically lowers the scientific risk, which is why so many companies are willing to invest in blocking these channels — they are chasing a target biology has already confirmed.

The opioid crisis created overwhelming demand for an alternative. Regulators, doctors, and insurers are desperate for effective pain relief that does not cause addiction. That demand pulls research forward and clears regulatory paths, as the swift approval of the first non-opioid class in decades demonstrated. The market and the public-health need are pointing in the same direction, which rarely happens and powerfully accelerates progress.

Chemistry has finally caught up with the biology. Sodium channels are notoriously similar to one another, so a drug that blocks the pain channel once risked blocking channels in the heart or brain. Advances in molecular design now let chemists build compounds precise enough to hit one channel and leave the rest alone. That selectivity, not the discovery of the target, was the real bottleneck — and it is finally breaking.

What Could Happen

What Can We Do

This shift will unfold over years, but patients, clinicians, and policymakers can prepare for a world where strong pain relief no longer means courting addiction.

Ask about non-opioid options for severe pain. As new channel-blocking drugs reach pharmacies, they will not always be offered first out of habit or cost. If you or a family member faces surgery or serious pain, ask your doctor whether a non-opioid alternative is appropriate. Informed patients speed the adoption of safer treatments.

Keep expectations honest. These drugs are a real advance, not a miracle. They may not erase every kind of chronic pain, and marketing will tempt overstatement. Judge them on evidence for your specific condition, and be wary of any claim that a single pill ends all pain — the biology is more complicated than that.

Support continued funding for pain research. The breakthrough here began with rare families and patient genetics that took years of unglamorous study. Public and charitable funding for that basic science is what makes new drug classes possible. It deserves sustained backing, especially given how much human suffering chronic pain represents.

Do not abandon opioids recklessly. For some patients, existing medicines remain necessary today. The goal is more options and safer defaults, not sudden withdrawal of relief from people who currently depend on it. Any transition should be guided by a clinician, not by headlines about a promising future.