It can rescue suppression of VGPC functions by regulating methylation of Kcna2 and K2p1.1 promoters in the neuropathic pain models.202,203 Restoration of PROX1 levels following TET1 overexpression attenuates depression comorbidity through neurogenesis enhancement.204 Some studies have claimed the opposite roles of TET1 in the same therapy.198,204 More strangely, the contradictory data are based on investigations into the similar pain types and model generation methods, reflecting the complexity of epigenetic modification in pain sensation. This evidence concerns the gene TET1 and major depressive disorder.