An important regulator of α4β1 is the BCR, and several studies have demonstrated that inhibiting the BCR-target BTK with ibrutinib abolishes the CLL adhesive and migratory function of α4β1 in tissues, a fact that correlates with the observed ibrutinib-induced lymphocytosis (209, 210) (Figure 2). This evidence concerns the gene BCR and B-cell chronic lymphocytic leukemia.