More recent data in prostate cancer suggest that the effects of PTEN loss on cell growth and response to PARP inhibition are context dependent [51]; in a series of in vitro and in vivo experiments using pten heterozygous, pten null, with or without tp53 loss, mouse embryonic fibroblasts (MEFs) or mice, it was demonstrated that in a p53 proficient setting, treatment of PTEN–deficient cells with PARP inhibitors leads to a senescence response. Here, TP53 is linked to prostate carcinoma.