These Nav1.7 mutations have been shown to be an underlying causation of a variety of neuropathic pain disorders such as small-fiber neuropathy (SFN), inherited erythromelalgia (IEM), and paroxysmal extreme pain disorder (PEPD), as well as the loss of pain exhibited by congenital insensitivity to pain (CID) [4,5,6,7]. Here, SCN9A is linked to paroxysmal extreme pain disorder.