PRRT2 and Hyperglycemia: Hyperglycaemia induced oxidative and nitrosative stress are essential steps in the pathogenesis of microvascular complications resulting in DNA damage, excessive poly (ADP-ribose) polymerase (PARP) activation, and inhibition of glyceraldehyde 3-phosphate dehydrogenase resulting in activation of aldose reductase, protein kinase C (PKC), the hexosamine pathway, and advanced glycation end products (AGE), all of which result in endothelial and microvascular dysfunction resulting in microvascular complications [22–24].