Finally, it is important to note that the two models for the function of the BRCA2–RAD51 interaction shown in Figure 2 are not mutually exclusive. BRCA2 could prevent inappropriate RAD51 assembly in the absence of damage and promote functional RAD51 assembly at DNA lesions during the damage response. Further experiments are clearly required to clarify the functional interactions between BRCA2 and RAD51 during recombinational repair. It should be relatively straightforward to determine whether the role of BRCA2 is limited to transporting RAD51 to the nucleus. If this were the case, addition of a nuclear localization signal to RAD51 should suppress the RAD51-mediated phenotypes associated with a BRCA2 mutation. However, biochemical experiments are needed to determine whether full-length BRCA2 blocks or promotes RAD51–BRCA2 interaction. Such experiments could also reveal additional roles for BRCA2 in recombinational repair. However, several technical obstacles, including the large size of BRCA2, promise to make biochemical characterization of BRCA2 function difficult.