In such competition, the persistent effects of the oncogenic alterations of MYC, HIF-1α, and the RAS/ERK and AKT/PI3K/mTOR pathways, which drive the upregulation of glycolysis and glutaminolysis, may endow cancer cells with a competitive advantage over immune cells, facilitating as a result the incapacitation of the T and NK cells through the depletion of nutrients in the TME [44, 65–68]. The gene discussed is MYC; the disease is cancer.