The increase in the histone deacetylation and histone methylation (H3K4me3 and H3K27me3) around the hypomethylated regions suggested that tumor cells could mobilize histone modifications to continue suppressing genes after DNA methylation was inhibited by the 5-azacytidine.740 Their work suggested that compensatory epigenomic alterations predominantly triggered by H3K27me3-based silencing following treatment-induced DNA methylation reduction, laying the groundwork for a potential DNMT and EZH2 inhibitor combination therapy in BRAFV600E CRC. The gene discussed is EZH2; the disease is neoplasm.