In summary, monotherapy with anti-PD-1 increases tumor MHC-I expression via increased T-cell reactivity and IFNγ production, while the addition of anti-CTLA-4 broadens immune reactivity which may further increase MHC-I expression; activation of type I IFN signaling, epigenetic drugs (DNMTi, HDACi, EZH2i) and radiation synergize with immunotherapy to increase tumor MHC-I expression and immune recognition, also providing a pathway to improved T-cell recognition in IFNγ-resistant tumors. This evidence concerns the gene IFNG and neoplasm.