It has been postulated that the excess generation of •O2− may be the initiation process of oxidative stress-induced diabetic complications like diabetic neuropathy through the overactivation of MAPK, PKC, and NAD(P)H oxidase [42]. In vitro studies on sensory neurons have revealed that high concentrations of glucose promote the mitochondrial-dependent pathway of apoptosis and oxidative stress [56]. Here, PRRT2 is linked to diabetic neuropathy.