However, because Fe-S cluster proteins such as XPD, polymerase delta, and FANCJ, which are down-regulated in the absence of SFXN4 (Fig. 4), are essential to the function of both NER and HRR repair, targeting SFXN4 may permit the simultaneous inhibition of multiple DNA repair pathways that contribute to resistance to DNA damaging drugs, thereby limiting the ability of ovarian cancer cells to restore DNA repair by shifting to compensatory repair pathways. This evidence concerns the gene BRIP1 and ovarian carcinoma.