NES and leukemia: 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.