MTOR and neoplasm: Factors such as Hypoxia-Inducible Factor 1-Alpha (HIF-1α), tumor suppressor gene inactivation, oncogene activation, noncoding RNAs, glycolysis-associated transporters and enzymes, and the phosphatidylinositol 3-kinase (PI3K)-Akt-mechanistic target of rapamycin (mTOR) signal transduction pathway may lead to tumor cells preferring glycolysis over mitochondrial oxidation (Figure 1).