While the role of Ref-1 and NF-κB and Ref-1’s redox signaling inhibition has been supported in other inflammatory model systems, as observed in the conversion of preleukemia to leukemia (45), inflammatory bowel disease (46), and retinal indications (47), the uniqueness of these studies is the use of a genetically modified murine KC cell model with functional mutation of NF-kB/RelA. Here, NFKB1 is linked to myelodysplastic syndrome.