Under hypoxic conditions, stabilization of hypoxia-inducible factor-1-alpha (HIF-1α) enhances overexpression of the PI3K–Akt–mTOR pathway and glucose transporters (e.g., GLUT-1) to reinforce glucose consumption and acidification of the tumor microenvironment (TME) [6,7,8,9]. The gene discussed is AKT1; the disease is neoplasm.