HDAC-mediated histone deactylation has well-recognized roles in cancers via transcriptional repression of tumor suppressor genes.92, 93 While some HATs are also putative tumor suppressors and inactivating mutations in p300/CBP have been identified in breast, colorectal and gastric cancers,94, 95 several fusion genes that involve HATs, such as MLL-CBP96 and MOZ-TIF297 behaves as oncogenic factors in hematological malignancies. This evidence concerns the gene HDAC9 and neoplasm.