It had previously been suggested that breast cancer type 2 susceptibility (BRCA2) forms a complex with Aurora B during cytokinesis and may thus have a role in abscission. Here, Couch and colleagues show that, during cytokinesis, BRCA2 is recruited to the midbody by interacting with the actin-binding protein filamin A. There, BRCA2 has a role in recruiting endosomal complexes required for transport (ESCRTs) and ESCRT-interacting proteins such as CEP55, which in turn mediate abscission. Importantly, mutations that inhibit binding of BRCA2 to filamin A disrupt localization of midbody components, and thus abscission, but have no effect on homologous recombination. So, this study confirms that BRCA2 plays a part in abscission that is independent of its role in DNA repair.