The causes of increased carcinogenic risk in diabetes include increased oxidative stress, high levels of insulin, related growth factors, and its binding factors, insulin receptor substrate-1 and their downstream phosphoinositide 3-kinase (PI3K), AKT, mitogen-activated protein kinase (MAPK) signal, AMP activated kinase (PRKA), mammalian target of rapamycin, sirtuin 1, and autophagy signal activation [2, 4–6, 11–13]. This evidence concerns the gene AKT1 and diabetes mellitus.