In estrogen-responsive breast cancer cells, this effect is probably reached through an increase in the levels of p53 and p21 in parallel with a downregulation of cyclin D1; p53 participates in growth suppression and apoptosis; the activation of p21 by p53 leads to a failure in phosphorylation of the retinoblastoma factor and cell cycle arrest [144]. Here, TP53 is linked to breast carcinoma.