NTRK1 and hereditary sensory and autonomic neuropathy: To date, the pathophysiologic mechanisms known to be implicated in HSAN include sphingolipid metabolism with mutations in SPTCL1 or SPTCL2 (serine palmitoyl-transferase genes), vesicular transport (RAB7, IKBKAP) or neurotrophic factors and their tyrosine kinase receptors (NTRK1, NGF-B) [6–8].