Multiple lines evidence support the mechanisms of suppressive effect on antitumor immunity by aerobic glycolysis by crosstalk of cytokines such as IFNs, programmed cell death 1 (PD-1)-ligand 1 (PD-L1), and serine/threonine kinase Akt in the tumor microenvironment, allowing cancers to resist the effects of endogenous tumor-specific T cells [4, 5, 18, 19]. Here, PDCD1 is linked to neoplasm.