Under shear flow conditions, immortalized or primary CLL cells with trisomy 12 (associated to high levels of LFA-1 and VLA-4) significantly arrested to endothelial cells or VCAM/ICAM-1 coatings in the presence of CCL21, but not of CXCL12, since only the CCR7 ligand was capable to induce inside-out VLA-4 conformational changes as demonstrated in real-time kinetic assays (14, 87). This evidence concerns the gene CXCL12 and B-cell chronic lymphocytic leukemia.