In mice, bone cancer pain and oxaliplatin-evoked mechanical and cold allodynia all occur normally in Nav1.7 null mutant mice.[1] In humans a recent case report suggests that individuals who carry loss-of-function mutations in SCN9A, associated with CIP, still have the potential of developing neuropathic pain.[39] Thus Nav1.7-targeted antagonists are not the panacea for all pain syndromes, despite the remarkably broad role of the channel in acute and inflammatory pain states. The gene discussed is SCN9A; the disease is hereditary sensory and autonomic neuropathy.