Previous studies have reported that the activation of IGF/IGF-1R signaling is essential for cancer initiation and progression through several distinct pathways, including phosphorylation of mitogen-activated protein kinase (MAPK), which subsequently increases cell proliferation, the activation of phosphatidylinositol 3′ kinase (PI3K), which decreases apoptosis, and the regulation of mammalian target of rapamycin (mTOR) expression, which results in translational adaptation [9,10]. The gene discussed is MTOR; the disease is cancer.