Given the availability of new and effective therapies that exploit the defect in homologous recombination, which exists in BRCA1-related cancers such as poly (ADP-ribose) polymerase (PARP) inhibitors [26] and Cisplatin [27], it will become increasingly important to determine whether the pathways leading to ER+ BRCA1 breast cancers are similar to those that result in ER- BRCA1 cancers and whether these new therapies are likely to be effective in ER+ BRCA1 cancers. The gene discussed is BRCA1; the disease is breast cancer.