A high level of H2A.Z expression is detected in many cancers and is significantly associated with cellular proliferation and genomic instability.[1] Histone variant macroH2A1 is important in the pathogenesis of many types of cancers, for instance in hepatocellular carcinoma.[28] Other mechanisms include a decrease in H4K16ac may be caused by either a decrease in activity of a histone acetyltransferases (HATs) or an increase in deacetylation by SIRT1.[9] Likewise, an inactivating frameshift mutation in HDAC2, a histone deacetylase that acts on many histone-tail lysines, has been associated with cancers showing altered histone acetylation patterns.[29] These findings indicate a promising mechanism for altering epigenetic profiles through enzymatic inhibition or enhancement.