This is consistent with previous studies reporting either additive or synergistic intertactions between p53 and ING1.23,26,30,31 It may result from the ability of ING1b to stabilize and modulate the activity of p53 and its target genes.32–34 Additionally, nine breast cancer cell lines that differed in p53 status and that showed different sensitivity to HDAC inhibitors (Supplementary Table S1 and data not shown) showed no obvious correlation between the levels of Ad-A3H-NLS/NTS-induced cell death, p53 status and sensitivity to HDAC inhibitors (data not shown). This evidence concerns the gene TP53 and breast cancer.