The second paper providing evidence, by Davies et al [26], is a biochemical study of the interaction between the homologous recombinase RAD51 and a peptide consisting of one of the eight BRC repeats from human BRCA2. Expression of a single BRC repeat (BRC4) had previously been reported to act as an inhibitor of DNA repair by Chen et al [27]. These investigators showed that expression of constructs containing the BRC4 repeat in MCF-7 cells enhances the radiosensitivity of cells and blocks both the G2/M delay associated with damage and the ability of the transfected cells to assembly subnuclear RAD51 foci. In the paper by Davies et al, data provide evidence for a plausible mechanism of the dominant negative effect associated with expression of a single BRC repeat. DNA binding assays and electron microscopy methods were used to show that a BRC3 peptide interferes with the ability of RAD51 to assemble into oligomeric filaments on DNA. A BRC4 peptide was also reported to inhibit the RAD51–DNA interaction. These experiments raise the possibility that the full-length BRCA2 protein could act as a negative regulator of inappropriate RAD51–DNA interaction.