Moreover, phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin signaling, often hyperactivated by insulin and IGF-1 in the diabetic state, contributes to the metabolic reprogramming of prostate cancer cells, inhibition of autophagy, and progression to castration-resistant disease by coordinating nutrient sensing with unchecked growth and anti-apoptotic responses [15,16]. This evidence concerns the gene IGF1 and Familial prostate cancer.