Gain-of-function missense variants in SCN9A lead to extreme pain perception with autosomal dominant transmission (primary erythermalgia, OMIM 133020 or paroxysmal extreme pain disorder, OMIM 167400), whereas non-sense variants with subsequent loss-of-function NaV1.7 channels cause autosomal recessive congenital insensitivity to pain (insensitivity to pain, congenital CIP/neuropathy, hereditary, sensory, and autonomic type IID, OMIM 243000) (Hisama et al., 1993; Majeed et al., 2018). The gene discussed is SCN9A; the disease is neuropathy.