Taken together, we suggest that BM TNF-α is a critical factor in the onset and subsequent progression of irradiation-induced BM dysfunction with clinical features of secondary MDS (shown in vitro and in vivo), and as such, strategies designed to block the effects of TNF-α in the BM microenvironment may be an attractive option to treat patients with secondary MDS. This evidence concerns the gene TNF and myelodysplastic syndrome.