EZH2 and neoplasm: By integrating scRNA-seq with single-cell assay for transposase-accessible chromatin using sequencing (scATAC-seq) profiles from primary tumors—followed by bulk CUT&Tag and ATAC-seq after EZH2 knockdown—the study showed that the CSC subpopulation enriched in recurrent cancers sustains stemness through EZH2-mediated deposition of H3K27me3 that keeps the tumor-suppressive cell-adhesion gene NCAM1 transcriptionally silent [46].