Given that CHO cells deficient for RAD51C, RAD51D, XRCC2 or XRCC3, and human HCT116 cells deficient for XRCC3 are viable, we attempted to disrupt each classical RAD51 paralog individually in transformed human osteosarcoma U2OS and human embryonic kidney HEK293 cells. This evidence concerns the gene XRCC3 and osteosarcoma.