The gene was an interesting candidate because of (i) its central role in recombination and DNA repair, (ii) its physical interaction with the two well known breast cancer susceptibility products BRCA1 and BRCA2 that activate a DNA damage response pathway involving both recombination and double-strand break repair and (iii) the identification in breast and/or ovarian cancer families of germline deleterious mutations in three of its five paralogs, RAD51C, RAD51D, and XRCC2[15], [39]-[42]. This evidence concerns the gene RAD51D and ovarian cancer.