That prevailing view greatly influenced how researchers assessed p53 function over the years since nearly all studies of p53 acetylation (and other post-translational modifications) focused on how they affected p53 transcriptional control of cell cycle inhibitory and apoptotic genes, like p21 and Puma. Indeed, one of the most compelling findings supporting a critical role for p53 acetylation in tumor suppression was the inability of an acetylation-deficient p53 mutant (8KR) to induce cell cycle arrest or apoptosis [40]. Here, CDKN1A is linked to neoplasm.