Of relevance to the role of NaV1.7 in pain, we found that CRMP2K374A/K374A mice of both sexes failed to develop mechanical allodynia after a spinal nerve injury (SNI) [37], thus supporting the conclusion that CRMP2 SUMOylation-dependent regulation of NaV1.7 still holds in chronic neuropathic pain in male mice. The gene discussed is SCN9A; the disease is Pain.