[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. The gene discussed is CXCL12; the disease is acute myeloid leukemia.