In a variety of tumor cells, Glut1-dependent enhancement of glycolysis was shown to counteract CTL-mediated cytotoxic effects by reducing ROS production and downregulating c-FLIP, a key inhibitor of TNF-α-induced cell death, and targeting Glut1 contributed to the improvement of tumor immune infiltration and sensitivity to ICB therapy (Wu et al., 2023). The gene discussed is TNF; the disease is neoplasm.