For example, treatment of pre-B ALL cell lines or primary samples with SDF-1α, which causes activation and internalization of CXCR4, resulted in increased adhesion to fibronectin, laminin, and VCAM-1, suggesting that SDF-1α and CXCR4 influence the functionality of VLA-4.[28] Another study showed that treatment of neutrophils with SDF-1α also led to increased adhesion to VCAM-1.[29] Therefore, it is possible that the pattern in organ-specific surface expression of CXCR4 and CD49d in control-treated mice is part of a homeostatic relationship. The gene discussed is FN1; the disease is acute lymphoblastic leukemia.