Two recent papers provide new evidence relevant to the role of the breast c
ancer susceptibility gene BRCA2 in DNA repair. Moynahan et al provide genet
ic data indicating a requirement for BRCA2 in homology-dependent (recombina
tional) repair of DNA double-strand breaks. The second paper, by Davies et
al, begins to address the mechanism through which BRCA2 makes its contribut
ion to recombinational repair. BRCA2 appears to function in recombination v
ia interactions with the major eukaryotic recombinase RAD51 [1-3]. We brief
ly review the context in which the two studies were carried out, we comment
on the results presented, and we discuss models designed to account for th
e role of BRCA2 in RAD51-mediated repair.