In these models, mammalian target of rapamycin (mTOR) and 5′ adenosine monophosphate-activated protein kinase (AMPK) were both activated in tumor-reactive T cells, and the activation of these related signals by low-molecular weight compounds increased the therapeutic efficacy of PD-1-blocking antibody therapy (Fig. 3). This evidence concerns the gene PDCD1 and neoplasm.