One of the proposed mechanisms of DME is that hyperglycemia causes abnormalities of biochemical pathways, i.e., it induces different, overlapping metabolic pathways—the polyol pathway, formation of advanced glycation end-products (AGEs), and activation of protein kinase C (PKC)—and thus initiates the development of a cascade that culminates in the development and progression of diabetic retinopathy [11,12]. This evidence concerns the gene PRRT2 and Hyperglycemia.