While most currently available SAM-competitive and allosteric PRC2 inhibitors selectively target EZH2 with lesser potency for inhibition of EZH1 activity (Lee et al., 2018), our data suggest that inhibitors that effectively target both EZH2 and EZH1 catalytic activity may more effectively induce MHC-I expression in MHC-I low cancers. This evidence concerns the gene EZH1 and cancer.