In contrast, a recent study in breast cancer cell lines that were exposed to cisplatin in combination with inhibitors of either Ref-1/APE1 repair or Ref-1/APE1 redox activity, cisplatin resistance increased.245 The authors conjecture that a concurrent downregulation of mismatch repair proteins (MSH2, MSH6, MLH1, and ERCC1) may explain why those results differ from the other studies that demonstrate a greater response to cisplatin when Ref-1/APE1 is inhibited concurrently. This evidence concerns the gene APEX1 and breast carcinoma.