Despite this commitment to osteoblastic lineage, these mice show a lack of terminally differentiated OBs and deficient bone mineralization.83 Similar results were reported also for a JAK2V617F-MPN mouse model, in which sympathetic neuropathy causes a reduction of Nestin+ MSCs, which promotes the expansion of mutant HSCs and facilitates disease progression by loss of HSC-retention factor expression, including CXCL12, SCF, ANGPT1, and VCAM1.84 Frisch and colleagues81, using an immunocompetent murine model of leukemia, demonstrated that AML blasts alter directly normal OB functions. This evidence concerns the gene CXCL12 and acute myeloid leukemia.