The combined findings suggest that in LR-MDS, activation of NF-κB occurs in both hematopoietic and mesenchymal cells, likely through autocrine and paracrine feedback signaling networks, leading to a NF-κB-mediated inflammatory milieu in the LR-MDS bone marrow and an overexpression of a repertoire of secreted negative hematopoietic regulators. This evidence concerns the gene NFKB1 and myelodysplastic syndrome.