Specifically, we analyzed the enrichment of histone H3 acetylated at lysines 9 and 14 (H3K9K14ac), and trimethylated at lysine 4 (H3K4me3) upon treatment of breast carcinoma cell lines with MS-275, a well-known histone deacetylase (HDAC) inhibitor able to induce chromatin hyperacetylation (Fig. 4e,f)31. Here, HDAC9 is linked to breast carcinoma.