CD274 and neoplasm: Two underlying mechanisms are involved: (i) binding of PD-1 receptors to PD-L1 ligands on T cells, which are overexpressed on tumor cells, leading to T-cell exhaustion; (ii) CTLA-4 competitively binds to cluster of differentiation (CD)80/CD86 co-stimulatory molecules, thereby inhibiting early-stage T-cell activation [11].