Proposed mechanisms by which mitochondrial dysfunction occurs in diabetic retinopathy include chronic hyperglycemia stimulating the production of sorbitol via the polyol pathway, advanced glycation end products (AGEs), and other toxic pro-inflammatory metabolites via the diacylglycerol protein kinase C (DAG-PKC) pathway (47–49). The gene discussed is PRRT2; the disease is diabetic retinopathy.