A model to explain anti–VLA4/VCAM-1—induced mobilization. Normally there is strong adhesion of hematopoietic cells to stromal endothelial cells through the VLA4/VCAM-1 pathway, which overrides any positive effects of kit on migration of stem/progenitor cells expressing kit. Consequent to antifunctional antibody treatment, there is deadhesion, which, either indirectly (by relieving the negative pressure on kit) or directly through communicating molecules, activates kit with ensuing stimulation of migration. During this process cells that are ready to egress downmodulate both α4 and kit. It is likely that increased migration via a kit-dependent pathway is achieved by activation/deactivation of another integrin to provide mechanistic support of cell movement. This effect may be strengthened by alleviation of a transdominant effect that VLA4 may exert on other integrins.