Increased ROS production due to chronic hyperglycaemia and mitochondrial dysfunction escalates oxidative stress after activation of metabolic pathways, including glucose autooxidation, with the enhanced formation of advanced glycation end products (AGEs), deactivation of the insulin signalling pathway, activation of the polyol pathway, hexosamine pathway, and protein kinase C (PKC) (38, 41, 42). The gene discussed is INS; the disease is Hyperglycemia.