Breast cancer, the second most common cancer in the United States, can result from a number of cellular misregulations, such as deficiencies in the DNA-repairing breast cancer gene, BRCA. Typically, BRCA-associated breast cancer is treated with poly ADP ribose polymerase (PARP) inhibitors and, recently, clinical trials have investigated pairing PARP inhibitor therapy with immunotherapy. Based on preclinical data, it is expected that the combination will recruit and activate T cells—immune cells that can kill tumor cells. Despite interest in this combination, researchers are already looking ahead for ways to get even more benefit from PARP inhibitors plus checkpoint inhibitors in breast cancer patients. That is precisely what a team of Dana-Farber/Brigham and Women's Cancer Center researchers have devoted their time to: identifying ways to boost the response to PARP inhibitors. The team found macrophage-mediated immune suppression to be the weak spot of PARP inhibition treatment. Findings are published in Nature Cancer.