EZH2 and cancer: These effects were conserved in multiple MHC-I low cancers and pharmacological inhibition of PRC2 using either SAM-competitive EZH2 inhibitors (EZH2i) or EED-226, an inhibitor that blocks H3K27me3 binding and allosteric activation of EZH2, markedly amplified IFN-γ-induced MHC-I upregulation (Figures 3B–3D, S3B, and S3C) (Qi et al., 2017) and reduced the threshold concentration of IFN-γ required to induce MHC-I gene expression (Figures 3E and S3D).