MVs with NH(2)-terminal truncation of the CXCR4 molecule are capable of transferring the CXCR4 molecule to AML-derived HL-60 cells, enhancing their migration to SDF-1 in vitro and increasing their homing to the bone marrow of irradiated NOD/SCID/beta2m (null) mice. The gene discussed is CXCL12; the disease is acute myeloid leukemia.