Ectopic expression of wild-type PAI-1 in breast cancer cells or in p53-deficient murine and human fibroblasts, in fact, initiates a senescence-like growth arrest [92, 107] while RNAi-mediated PAI-1 knockdown (PAI-1KD) or PAI-1 genetic deficiency (PAI-1−/− genotype) results in escape from replicative senescence in primary mouse and human fibroblasts [107]. This evidence concerns the gene SERPINE1 and breast carcinoma.