Cancer is accompanied by an abnormal activation of PI3K, HIF-1A, RAS, MYC, and other pathways that activate nuclear factor kappa B subunit (NFκB) and mechanistic target of rapamycin kinase (mTOR) by facilitating GLUT1 overexpression and participate in cell proliferation, metastasis, and chemotherapy resistance (28, 30–32). The gene discussed is HIF1A; the disease is cancer.