Homozygous or compound heterozygous loss-of-function mutations in Nav1.7 lead to congenital insensitivity to pain (CIP)2,5,6, whereas gain-of-function mutations cause episodic pain (i.e., primary erythromelalgia and paroxysmal extreme pain disorder) in humans7–9. Here, SCN9A is linked to hereditary sensory and autonomic neuropathy.