Diabetic retinopathy (DR) has traditionally been considered to be a microcirculatory disease caused by the deleterious metabolic effects of hyperglycemia per se and the metabolic pathways triggered by hyperglycemia, including the polyol (50), hexosamine, and diacylglycerol-protein kinase C (DAG-PKC) pathways (51, 52), that result in advanced glycation end-products (53) and the induction of oxidative stress (54). This evidence concerns the gene DAG1 and Hyperglycemia.