The interaction of PD-1 with PD-L1 and PD-L2, which are expressed prevalently in NSCLC, downregulates T cell activation and promotes tumor immune escape.[7–9] Anti-PD-1/PD-L1 therapy uses PD-1/PD-L1 immune-checkpoint-inhibitor antibodies to disrupt PD-1/PD-L1-mediated signaling and restore antitumor immunity. Here, CD274 is linked to neoplasm.