Subsequently, hyperglycemia-induced superoxide anions and hyperglycemia induce the flux of mitochondrial electron transport chain through four damaging pathways [generation of advanced glycation end-products (AGEs), protein kinase C (PKC) activation, polyol formation and hexosamine pathway stimulation], thus supporting the hypothesis that mitochondrial-derived ROS is the missing link to the glucose disturbance observed in diabetes (7). The gene discussed is PRRT2; the disease is Hyperglycemia.