Within this context, hyperglycemia promotes massive cellular production of ROS in these tissues by stimulating glucose auto-oxidation, scavenging GSH, glycation, and suppression of antioxidant enzymes, impairing the mitochondrial oxidative phosphorylation, ketoacidosis, and activating several ROS-generating pathways, including AGEs, hexosamine phosphate, and PKC)/NADPH oxidase pathway [29]. This evidence concerns the gene PRRT2 and Hyperglycemia.