VCAM1 and precursor B-cell acute lymphoblastic leukemia: Natalizumab has been demonstrated to drastically diminish stromal adherence in primary B-ALL cells, making them susceptible to chemotherapy and increasing the survival of B-ALL-bearing animals [120] when paired with multi-agent chemotherapy that included dexamethasone, L-asparaginase, and vincristine, natalizumab dramatically extended survival in a xenograft model of B-ALL compared to chemotherapy alone, according to Hsieh et al. Other treatment strategies include peptide or nonpeptide ligands that outbid VCAM-1 for binding to VLA-4.