Therefore, we speculate that the pathogenic factors of the IGT stage (hyperinsulinemia and hyperglycemia) can affect the function of capillary endothelial cells through the PI3K/Akt/eNOS and MAPK/ET-1 pathways, and participate in the progress of renal tubular ischemia and hypoxia, leading to IGT nephropathy. The gene discussed is NOS3; the disease is hyperinsulinism.