SCN9A and paroxysmal extreme pain disorder: Its key role in human pain signaling is impressively demonstrated by loss-of-function Nav1.7 mutations causing congenital insensitivity to pain [2], while gain-of-function mutations lead to severe painful disorders, such as inherited erythromelalgia (IEM) [3], paroxysmal extreme pain disorder [4], or small fiber neuropathy (SFN) [5].