The mechanism may be as follows: activate pancreatic β-cell NFκB signaling pathway, cause cell inflammation, induce cell apoptosis, and inhibit insulin secretion; acts on insulin signaling pathways such as InsR, IRS, PI3K, Akt, GLUT, and induces insulin resistance in liver, muscle, and adipose tissue; the injury causes the accumulation of advanced glycation end products and promotes the occurrence and development of late complications of T2DM.[19]. The gene discussed is AKT1; the disease is type 2 diabetes mellitus.