This interferes with the ability of p53 to induce apoptosis via transcriptional transactivation of many pro-apoptotic genes, particularly BAX, PUMA and NOXA. Nevertheless, HDACi can stimulate apoptosis independently of p53 and similarly to p53, hyperacetylation of RUNX3 by HDACi increases stability and transcriptional activity, thereby leading to cell cycle arrest and apoptosis by transcriptional upregulation of p21 and Bim in tumor cells [108,165,166]. This evidence concerns the gene TP53 and neoplasm.