Chronic pain affects millions, but opioid painkillers bring addiction, tolerance and fatal breathing risks. The voltage-gated sodium channel Nav1.7, encoded by SCN9A, is key in pain signaling. 2004 research linked its gain-of-function mutations to primary erythromelalgia, and 2006 work connected loss-of-function mutations to congenital insensitivity to pain, making it a therapeutic target. Though Nav1.7 inhibitor development faced challenges, 2025’s FDA approval of Nav1.8 inhibitor suzetrigine, a milestone in non-opioid analgesia, showing genetics’ role in advancing medicine. (By Pu Xia, https://jmg.bmj.com/content/early/2025/09/11/jmg-2025-111174 )

Group Photo of the Genetic Skin Disease Center, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs