The decreased glucose availability resulting from metabolic changes associated with energetic stress induced by cancer development has been associated with an increase in the expression of stress response genes, including phosphoinositide 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR), mitogen-activated protein kinases, p53, and components of inflammatory cytokine signaling pathways [54]. This evidence concerns the gene MTOR and cancer.