PPARGC1A and neoplasm: The combination of anti-PD-L1 monoclonal antibody and oltipraz or bezafibrate, two ligands of the PGC1α/Nrf2 and PGC1α/PPAR complexes, respectively, resulted in augmented tumor-suppression activity compared to either treatment alone, explained by the significant increase in both mitochondrial metabolism and glycolysis, driven by PGC1α/PPAR signaling [105].