Higher insulin levels are responsible for stimulating the insulin/IGF-1R signaling pathway via serine phosphorylation of insulin receptor substrates (IRS), which, in turn, leads to the activation of the phosphatidyl inositol-3 kinase and mammalian target of rapamycin (PI3K/mTOR) pathway [29]. Frasca et al. and Kornmann et al. in their studies suggested that IGFR-1 and chronic hyperinsulinemia play a vital role in favoring cancer initiation, malignant transformation, and metastasis of various types of cancer in patients with diabetes [30,31]. The gene discussed is IGF1R; the disease is cancer.