This deviating effect in MCF7 may be a cell-type specific effect of the presence of p53, which plays a major role in CDKN1A trans-activation and/or could be explained by the possible involvement of breast cancer oncogenes PRMT6 [45] and FHL2 [46], as well as IGFBP-rP1 [47], which comprise p53-independent mechanisms of p21 control. This evidence concerns the gene RP1 and breast carcinoma.