Mutations in SCN9A, the gene encoding NaV1.7, which lead to a loss of function, result in congenital insensitivity to pain (CIP) with anosmia as the only other sensory deficit, whilst gain-of-function mutations are associated with extreme sensitivity to pain (erythromelalgia and paroxysmal extreme pain disorder) [3, 4]. This evidence concerns the gene SCN9A and Kallmann syndrome.