Recent evidences, reviewed by Pleyer et al. [34], show that MDS cells are heavily dependent on their “dysplastic niche.” MDS-derived MSCs display enhanced supportive capacities for clonal hematopoiesis by decreased expression of cell surface molecules [35], including CD44 and CD49e (α5-integrin) [36]. The gene discussed is ITGA5; the disease is myelodysplastic syndrome.