Tumor progression during cancer immunotherapy is the result of immunoselection by host immunity, and our findings suggest possible mechanisms of tumor escape from host immunity during immunotherapy via IFNγ‐induced overexpression of PD‐L1 and MHC class I molecules, and IFNγ‐induced down‐regulation of NKG2D ligands. This evidence concerns the gene KLRK1 and neoplasm.