In U2OS human osteosarcoma cells, PCAF and acetylation of H3K9 and H3K14 at the promoter of the cyclin-dependent kinase inhibitor p21 was found to be required for the p53-dependent transcriptional activation of p21 in response to the p14ARF tumor suppressor, MDM2-p53 interaction inhibitor treatment, and genotoxic stress [39]. This evidence concerns the gene TP53 and osteosarcoma.