On a molecular basis, the PI3K–AKT–mTORC1 pathway has been found to significantly contribute to the high glycolytic activity of many tumor cells.42 AKT directly and indirectly—by the activation of mTOR, which promotes the stabilization of the transcription factor hypoxia-inducible factor-1α—stimulates the expression of glucose transporters and key glycolytic enzymes (Figure 3). This evidence concerns the gene MTOR and neoplasm.