Concerning the involvement of NFkB, TNF-α has been shown to exert some of its effects via NF-kB [35], [36] The increase in NFkB p65 in 3x irradiated mice suggests this may be a molecular event involved in BM dysfunction and possibly progression to an MDS-like phenotype with increased likelihood of developing acute leukemia. The gene discussed is NFKB1; the disease is myelodysplastic syndrome.