We show here that Tregs with deficiency in NAC1 have enhanced metabolic capacity to adapt to the acidic TME, primarily through CD36/PGC-1α–driven enhancement of mitochondrial fitness and lipid metabolism, and NAC1-deficient Tregs promote tumor growth by increasing their tumor infiltration and strengthening their suppressive function within the TME (Figure 7D). This evidence concerns the gene PPARGC1A and neoplasm.