They found that HLA-DR expression in cancer cells correlated with response to anti-PD1 therapy and showed by mechanistic experiments that overexpression of CIITA, a master regulator of the MHC-II pathway, in anti-PD1 resistant cells resulted in HLA-DR expression and increased T cell infiltration, whereas loss of CIITA in anti-PD1 responsive cells resulted in reduced HLA-DR expression and decreased T cell infiltration. Here, CIITA is linked to cancer.