Although we cannot formally exclude that during in vivo homing high CD49d levels can partially compensate for decreased CXCR4 receptor densities in tri12 CLL, in vitro assays argue that these expressional CXCR4 differences are not decisive for the extent of CXCL12-induced arrests under shear flow (Supplemental Figure 4). This evidence concerns the gene ITGA4 and B-cell chronic lymphocytic leukemia.