The HDAC family members including HDAC1 are overexpressed in multiple cancer types and several HDAC inhibitors have been approved for cancer treatment.[24] HDAC inhibitors, including trichostatin A (TSA), valproic acid (VPA), sodium butyrate, and SAHA, can upregulate acetylated p53 and induce growth arrest and apoptosis,[3, 25, 26, 27] suggesting that HDAC‐mediated deacetylation acts as an important mechanism for p53 inactivation and tumor growth. The gene discussed is TP53; the disease is neoplasm.