The tumor suppressor gene p53, mutated in ≈50% of all human cancers, encodes a sequence-specific DNA-binding transcription factor. Target genes can be roughly categorized into two groups: genes that temporarily halt cell-cycle progression and genes that promote apoptosis. However, the molecular mechanism by which p53 senses whether to initiate cell-cycle arrest or apoptosis following cellular stress remains unknown. Here, we argue that the breast cancer tumor suppressor gene product BRCA1 might function as a molecular scaffold, assembling proteins involved in the fine-tuning of the p53 response.