Researchers have demonstrated a molecular strategy they say could make a much larger variety of tumors treatable with PARP inhibitors, a promising new class of cancer drugs. They report that the BRCA1 repair protein is dependent on the protein CDK1. When the scientists blocked CDK1 in cancer cell lines and in a mouse model of lung cancer, BRCA1 function was disrupted, making them susceptible to being killed by a PARP inhibitor.