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final experiment reported by Davies et al [26] is particularly important with respect to understanding the mechanism(s) through which BRCA2 promotes RAD51-dependent recombination. The localization of RAD51 was examined in CAPAN-1 cells, the same human tumor line examined by Moynahan et al [24]. It had been shown previously that the small amount of truncated BRCA2 protein expressed by CAPAN-1 cells was mislocalized to the cytoplasm, consistent with the fact that the truncation protein lacks a nuclear localization signal [28]. Davies et al showed CAPAN-1 cells to be defective in nuclear localization of RAD51, raising the possibility that RAD51 is normally carried to the nucleus by binding BRCA2. It is possible that RAD51 may alternatively be capable of BRCA2-independent transport, but mislocalization of BRCA2 to the cytoplasm may sequester RAD51 and block its normal mode of transport. Support for the hypothesis that the observed mislocalization of RAD51 is an indirect consequence of the BRCA2 defect requires reintroduction of functional BRCA2 into CAPAN-1."}