CRMP2-targeted therapies have been explored in multiple sclerosis mouse models to some success, and have been used to relieve chronic neuropathic pain by blocking CRMP2’s binding to calcium voltage-gated channels [22–24] or by allosteric regulation of voltage-gated NaV1.7 channels by CRMP2 [25–27]. The gene discussed is DPYSL2; the disease is multiple sclerosis.