Mutations of SCN9A that result in NaV1.7 gain-of-function underlie paroxysmal extreme pain disorder (PEPD) and primary erythromelalgia6, 7, whereas mutations that result in the loss of NaV1.7 function underlie ‘congenital insensitivity to pain’ (CIP)8. This evidence concerns the gene SCN9A and hereditary sensory and autonomic neuropathy.