In tumor patients, the production of VEGF-A in the tumor microenvironment enhances the expression of PD-1 and other inhibitory checkpoints associated with CD8 + T-cell exhaustion, which is reversed by anti-VEGF/VEGFR therapy and enhances the antitumour effects of anti-PD-1/PD-L1 antibodies [54]. The gene discussed is CD8A; the disease is neoplasm.