As we and the others have shown that RAD51 loading at damage sites can be mediated by BRCA2-independent mechanisms (11, 27), it will be interesting to investigate whether hyperactivation of the CK2–HTATSF1–TOPBP1 axis could contribute to HR reacquisition in BRCA2-deficient breast tumors and whether this type of tumor is synthetically lethal with strategies targeting the CK2–HTATSF1–TOPBP1 axis. The gene discussed is BRCA2; the disease is neoplasm.