Those currents can be altered by nerve injury [47] and such changes could contribute to neuropathic pain, but any association with primary afferent hyperexcitability is likely to be purely correlative and therapies targeting those currents would be ineffective at reversing hyperexcitability; however, the analgesic efficacy of gabapentenoid drugs acting on the α2-δ subunit of Cav1 and 2 channels [48], [49] clearly implicates other mechanisms as critical factors for pain processing. The gene discussed is ATXN2L; the disease is injury.