KMT2A and cancer: Given that bivalent H3K4me3 and H3K27me3-marked promoters are prone to acquiring aberrant DNA hypermethylation during cellular transformation [14, 26], coupled with our finding that PRC2 and MLL/COMPASS function to restrict DNA methylation, particularly at CGI, we asked whether loci commonly hypermethylated in cancer cells are disproportionately hypermethylated in our MLL/COMPASS- and PRC1/PRC2-depleted cells.