The deletion of the ribonuclease III enzyme Dicer1 from mouse osteoprogenitors, through the use of Cre recombinase driven by the osterix promoter (Osx‐Cre), led to myelodysplasia (MDS) (reduced blood cell counts with abnormalities detected in at least one blood cell lineage) and phenotypes typical of acute myeloid leukemia (AML), such as the accumulation of immature blood cells.(46) On the other hand, this was not observed when Dicer1 was deleted from mature OBs, by using a Cre recombinase driven by the osteocalcin promoter. The gene discussed is SP7; the disease is myelodysplastic syndrome.