Targeting metabolic enzymes offers promising therapeutic avenues: inhibition of lactate dehydrogenase A (LDHA) reduces lactate accumulation, reverses CD8+ T-cell dysfunction, and remodels the high-glucose, low-lactate microenvironment [158]; glutaminase (GLS) inhibitors disrupt tumor metabolic dependence, synergize with immune checkpoint blockade, and enhance CAR-T cell infiltration and efficacy [159]. This evidence concerns the gene GLS and neoplasm.