Ex vivo expanded patient-derived BM-MSCs were larger and disorganized, more senescent and had defective growth potential as compared to HD-derived BM-MSCs. MDS-derived BM-MSCs had reduced osteogenic potential, impaired expression of chemokines and molecules involved in hematopoiesis and defective hematopoietic support, such as Osteopontin, Jagged1, Kit-ligand and Angiopoietin as well as several chemokines. Patient and HD-derived BM-MSCs had differential methylation patterns showing enrichment for biological processes associated with cellular phenotypes and transcriptional regulation. This evidence concerns the gene KITLG and myelodysplastic syndrome.