Both HIF1-α and STAT3 have been inherently difficult to target with specific inhibitors.12 To circumvent this targeting difficulty, we have focused on the protein, Redox effector factor-1 (Ref-1) that interacts and regulates STAT3 and HIF1-α DNA binding and subsequently activates transcription.13–15 Based on the importance of these two transcription factors in other MPNST studies, as well as multiple studies showing high expression levels of Ref-1 indicating decreased survival in a number of cancers,8 we investigated the impact of targeting either Ref-1 or STAT3 in MPNST cells. The gene discussed is HIF1A; the disease is cancer.