SCN11A encodes Nav1.9, a voltage-gated sodium channel that plays a critical role in nociceptive signaling and pain perception. The protein mediates sodium ion permeability in excitable membranes and is preferentially expressed in nociceptive primary sensory neurons of dorsal root ganglia and trigeminal ganglia 1. Nav1.9 is essential for membrane depolarization during action potentials in nociceptors, which serve as key relay stations for transmitting pain signals from the periphery to the central nervous system 2. Gain-of-function mutations in SCN11A cause painful conditions including familial episodic pain syndrome type 3 and hereditary sensory and autonomic neuropathy type 7 3. These mutations are associated with erythromelalgia and small fiber neuropathy, conditions characterized by severe episodic pain and neuropathic symptoms 45. Interestingly, while most Nav1.9 mutations lead to painful conditions, a few rare mutations have been reported to cause pain insensitivity 2. The channel's critical role in pain signaling, combined with its low expression in the central nervous system and heart, makes it an attractive target for developing novel analgesic drugs 6.