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). This evidence concerns the gene MYC and cancer.