The induction of MHC-I after RT occurs by a three-step mechanism, including a proteasome-dependent increase in cytosolic peptide levels, mTOR-dependent protein translation and induction of radiation-specific peptides.56 In addition to these cell intrinsic mechanisms of MHC-I induction, radiation-induced IFN-γ induces MHC-I upregulation.33 Of note, upregulation of MHC-I post-RT does not seem to be a universal mechanism, but it is confined to a fraction of tumor cell lines.57 Thus, RT could increase MHC-I levels in some tumors with low endogenous MHC-I to increase immune-mediated attack. This evidence concerns the gene IFNG and neoplasm.