In mouse tumor models, tumor immunogenicity, reflecting differential immune cell infiltration in the TME, correlates with responsiveness to PD-1 blockade.4 While immunogenic (hot) tumors such as B16 melanomas transfected to express neo-antigens are responsive to PD-1 blockade, weakly immunogenic (cold) Lewis lung carcinoma (LLC) tumors are refractory to PD-1 blockade.2–5 Thus, the LLC model recapitulates the poor clinical responses to PD-1 blockade observed in most patients with lung cancer. This evidence concerns the gene PDCD1 and lung carcinoma.