The insulin resistance stimulates the bioavailability of insulin-like growth factor-1 (IGF-1); the interaction between IGF-1 and its receptors induces the downstream activation of the Ras-Raf-MAPK and PI3K/Akt pathways, thus leading to increased cancer cell proliferation, and inhibition of apoptosis [17,18,19,61]. The gene discussed is AKT1; the disease is cancer.