Ex vivo expanded MDS-derived BM-MSCs displayed reduced clonogenic and proliferative potential but did not differ in terms of differentiation capacity or inhibition of T cell proliferation as compared to their normal counterparts. The production of TNFα, IL1β, IL6, VEGF, CXCL12 did not differ between patient and HDs BM-MSCs. Cultured MDS-derived BM-MSCs did not harbor the cytogenetic abnormalities present in hematopoietic cells but in 4/13 cases developed irrelevant chromosomal alterations (trisomies 5 and 7). The gene discussed is CXCL12; the disease is myelodysplastic syndrome.