In particular, Nav1.7 has recently emerged as a target of considerable interest, since loss-of-function mutations in SCN9A, the gene that encodes Nav1.7, are associated with congenital insensitivity to pain [7-9] and gain-of-function mutations have been linked to pain in erythromelalgia [10-13] and paroxysmal extreme pain disorder (PEPD) [14-16]. This evidence concerns the gene SCN9A and paroxysmal extreme pain disorder.