Typically, mutations present in inherited erythromelalgia patients cause a voltage-dependent shift of activation of NaV1.7 to more hyperpolarized potentials [24,25,26,27], corresponding to the β-scorpion toxin-like effects of OD1, whereas paroxysmal extreme pain disorder mutations generally delay the fast inactivation [28,29,30], corresponding to the α-scorpion toxin activity of OD1. The gene discussed is SCN9A; the disease is erythromelalgia.