In the tumor microenvironment, cancer cells or myeloid cells (68) outcompete CD8+ T cells for glucose via the Warburg effect (69), leading to lactate accumulation (70, 71), acidosis, and metabolic stress (72), by upregulate glucose transporters GLUT1 and GLUT3 (73, 74), or elevated glucose metabolism (75). This nutrient deprivation impairs T cell mitochondrial function, mTOR signaling (76, 77), and effector responses, while promoting exhaustion markers (PD-1, LAG-3) and epigenetic dysfunction (72, 78–80). Targeting this metabolic competition may enhance immunotherapy efficacy (81). The gene discussed is MTOR; the disease is neoplasm.