Interestingly, human genetic studies disclosed mutations in NaV1.7 and NaV1.9 channels leading to congenital insensitivity to pain, a rare condition characterized by lack of physical pain (Cox et al., 2006; Phatarakijnirund et al., 2016), while gain-of-function mutations in NaV1.6, NaV1.7, NaV1.8, and NaV1.9 lead to painful neuropathies such as trigeminal neuralgia and erythromelalgia (Drenth and Waxman, 2007; Faber et al., 2012; Huang et al., 2014; Grasso et al., 2016). The gene discussed is SCN11A; the disease is erythromelalgia.