In patients with normal intelligence showing a pattern of pain insensitivity restricted to the limbs rather than diffuse and no anosmia, mutations in PRDM12 should be considered.21 CIP patients with normal intelligence, hyperhidrosis, gastrointestinal dysfunction and mild muscular weakness, without anosmia, neuropathy, or cardiovascular dysautonomia could harbor SCN11A mutations.20 When CIP is associated with impaired cognitive development and anhydrosis, the underlying molecular defect could be in the NTRK1 gene.5 This evidence concerns the gene NTRK1 and Kallmann syndrome.