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. This evidence concerns the gene SCN9A and bone neoplasm.