The near universal dependence on p53 inactivation in BRCA1 mutant tumor progression suggests that this relationship might be therapeutically exploited.2,11 Examples of approaches to target TP53 mutations include inhibition of complementary cell cycle checkpoints mediated by WEE1 and Chk1, but these strategies only indirectly target p53 defect.12,13 A more attractive approach would be to directly restore wild type p53 function in a BRCA1 deficient breast cancer. This evidence concerns the gene TP53 and breast carcinoma.