Mutations in the SCN9A gene which lead to a gain of Nav1.7 function are associated with primary erythromelalgia [5] and paroxysmal extreme pain disorder [6], while mutations in the SCN9A gene which lead to a loss of Nav1.7 function are associated with congenital insensitivity to pain [7]. The gene discussed is SCN9A; the disease is sodium channelopathy-related small fiber neuropathy.