Ten years ago, a concerted effort from several labs resulted in the cloning of BRCA1, the first of two major hereditary breast/ovarian cancer predisposition genes. Since that time, BRCA1 has been linked to several key nuclear functions connected with the prevention of genomic instability. In particular, BRCA1 functions in concert with Rad51, BRCA2 and other genes to control double strand break repair (DSBR) and homologous recombination. Here, we reassess the role of BRCA1 and its associated proteins in this process.