As a proof of concept, MDS development was demonstrated in mice with osteoprogenitor-specific deletion of Sbds. This ultimately raised the question if a similar disease-driving mechanism can be found in human MDS or at least in patients with the rare Shwachman–Bodian–Diamond syndrome (SBDS) that is caused by SBDS mutations and characterized by skeletal abnormalities, pancreatic deficiency and myelodysplasia [35]. The gene discussed is SBDS; the disease is Myelodysplasia.