The first evidence that alterations of a specific BM stromal population represented by osteolineage cells can drive myeloid malignancies arose from the deletion of Dicer1, an RNAse III endonuclease, in osterix-expressing osteoprogenitors, which caused MDS-like disease with increased propensity to develop AML.56Dicer1 depletion in mature OCN-expressing OBs did not result in a hematopoietic phenotype. Here, SP7 is linked to acute myeloid leukemia.