Cancer cells can exploit this mechanism for immune evasion by overexpressing programmed cell death 1 ligand 1 (PD-L1), thereby promoting cancer development and progression through negatively regulating T-cell-mediated immune responses and suppressing migration, proliferation and effector function of T cells, eventually inducing T cell exhaustion, a dysfunctional state of T cells lacking effector function accompanied by an increased expression of inhibitory receptors [2]. Here, CD274 is linked to cancer.