First, loss-of-function mutation in the SCN9A renders nociceptors unable to respond to any noxious stimulus.8 Second, loss-of-function mutation in the NTRK1 leads to a failure of nociceptors to develop.9 Recently, a new form of CIP has been described, caused by mutations in an epigenetic regulator PRDM12. 10, 11 The phenotype of these patients was briefly annotated in the initial study. This evidence concerns the gene SCN9A and hereditary sensory and autonomic neuropathy.