Ex vivo expanded patient-derived BM-MSCs had irregular morphology, reduced proliferation and differentiation potential, decreased expression of hematopoietic factors and increased levels of IL6. MDS-derived BM-MSCs and especially HR-MDS-derived BM-MSCs were epigenetically deregulated and supported poorly HSPCs. Treatment of patient-derived BM-MSCs with AZA reversed their functional abnormalities and improved their capacity to support hematopoietic cells for in vivo engraftment. This evidence concerns the gene IL6 and myelodysplastic syndrome.