Therefore, we reason that p53 acetylation related to either TIP60 or SIRT1 may be crucial for this CBX8-induced inhibition of p53 because TIP60 often acts as a functional partner for CBX8 [23, 36–38], and CBX8 suppresses the stress-induced premature senescence of human breast cancer cells through cooperation with SIRT1 to suppress p53 acetylation [39]. This evidence concerns the gene KAT5 and breast carcinoma.