Here, we chose to use an anti–PD-1 antibody for 3 reasons: (a) meta-analyses of anti–PD-1 versus anti–PD-L1 treatment showed improved efficacy in non–small cell lung cancer (NSCLC) patients receiving anti–PD-1; (b) anti–PD-1 also allows for blockage of the PD-1/PD-L2 interaction, PD-L2 being a second ligand of PD-1, which when highly expressed in solid tumors has been shown to correlate with worse clinical outcome; and (c) anti–PD-1 inhibition complemented our genetic approach by targeting the receptor versus the ligand (40, 41). This evidence concerns the gene PDCD1LG2 and lung cancer.