BM-MSCs from LR-MDS patients exhibited activated NF-κB signaling leading to transcriptional upregulation of inflammatory molecules, including factors with a negative impact on hematopoiesis. In co-culture experiments, ex vivo expanded murine OP9 mesenchymal cells with constitutive NF-κB activation reduced normal HSPC numbers and function. This evidence concerns the gene NFKB1 and myelodysplastic syndrome.