Tumor cells excessively uptake glucose through GLUT1 (uptake rate is 20 times higher than normal cells), causing TME glucose concentration to drop to 0.1–0.5 mM, forcing CD8+ T cells to switch to fatty acid oxidation for energy, but their mitochondrial metabolic capacity is insufficient, ultimately leading to functional exhaustion [42]. The gene discussed is SLC2A1; the disease is neoplasm.