In 2006 James Cox and Geoff Woods found that loss-of-function recessive mutations in Nav1.7 resulted in congenital insensitivity to pain (CIP).[23] This dramatic discovery energized the field to focus on this particular sodium channel isoform for the development of new analgesic drugs that should, in principal, be side-effect free. This evidence concerns the gene SCN9A and hereditary sensory and autonomic neuropathy.