PRRT2 and Hyperglycemia: Recent data has shown that the persistent hyperglycemia leads to an increase in the activity of several pathways involved in the disease that contribute to oxidative stress: (1) auto-oxidation of glucose, (2) advanced glycation end-product (AGE) formation, (3) polyol pathway flux, (4) protein kinase C (PKC) isoforms activation and (5) mitochondrial dysfunction [5, 10, 48–50].