For example, Chamoto and colleagues reported in a preclinical study (44) that ROS, by activating both AMPK and mTOR phosphorylation and by augmenting PGC-1α (a downstream target of both AMPK and mTOR known to increase mitochondrial activity), strongly activated mitochondrial function in tumor-reactive T cells and showed synergistic tumoricidal effects with PD1 blockade. This evidence concerns the gene PPARGC1A and neoplasm.