This is perhaps not surprising since metabolism is an Achilles' heel in cancer biology [41]; For instance, aberrant PI3K/AKT pathway during cancer development inadvertently amplifies glucose metabolism and translational activities via glucose transporter (GLUT4), mTOR/S6K/eukaryotic initiation factor 4E-binding protein 1 (4EBP-1), respectively [42], [43]. The gene discussed is AKT1; the disease is cancer.