Furthermore, the mechanism of Schwann cell involvement in DPN pathogenesis is considered to be sustained hyperglycemia, which leads to increased fluxes of polyol pathways in Schwann cells; a decrease in the production of neurotrophic factors, such as myelin, ciliary neurotrophic factor (CNTF), nerve growth factor (NGF), and neurotrophin-3 (NT-3); mitochondrial dysfunction; oxidative stress; altered lipid metabolism; the release of inflammatory factors that bring about neuroinflammation; axonal demyelination; and slow nerve conductive velocity (NCV), which in turn promotes DPN progression [8]. The gene discussed is CNTF; the disease is Hyperglycemia.