The risk of DN is tightly linked to poor glucose control in both type 1 and type 2 diabetes, which is associated with hyperglycemia [5, 6], and the impacts of hyperglycemia are generally mediated through diverse metabolic pathways, including increased reactive oxygen species formation, excessive production of advanced glycation end products (AGEs), and the activation of the polyol, protein kinase C (PKC), and hexosamine pathways [7]. This evidence concerns the gene PRRT2 and Hyperglycemia.