The key role of both BTK and PI3K in the induction of VLA-4 activation was also observed in normal B cells from healthy donors (Fig. S1 B), where, similarly to what we reported in CLL cells, only concomitant inhibition of both BTK and PI3K was able to abrogate anti-IgM–induced VLA-4 activation. This evidence concerns the gene BTK and B-cell chronic lymphocytic leukemia.