The emerging consensus is that MHC-II directly presents tumor antigens to activate CD4+ T cells within the tumor microenvironment, and the requirement for MHC-II-mediated CD4+ T cell activation in PD1 inhibitor responses has been confirmed in non-small cell lung carcinomas and classical Hodgkin’s lymphoma45,48. This evidence concerns the gene PDCD1 and non-small cell lung carcinoma.