[27] Patients whose AML blasts express low surface VLA-4 had better response to chemotherapy and improved survival suggesting that the VLA-4 pathway may also play a role in mediating resistance to chemotherapy similar to the CXCR4/SDF-1 axis. [28] Our in vitro data, however, suggest that binding of APL cells to plate bound fibronectin had no impact on the sensitivity of APL cells. This evidence concerns the gene CXCR4 and acute myeloid leukemia.