Our previous studies demonstrated that STAT3 is under Ref-1 redox control in other cancers including pancreatic cancer.15 In addition, Rad et al.’s study in MPNST revealed the importance of STAT3 and HIF1-α in driving MPNST phenotype.5 Although STAT3 is regulated through Ref-1-dependent redox activity, there are several other forms of STAT3 regulation including phosphorylation and nuclear translocation. Here, HIF1A is linked to familial pancreatic carcinoma.