In this blood compartment and in the context of BCR‐autonomous signaling, in contrast to the situation of antigen stimulation within the lymph node microenvironment, ibrutinib is capable of interfering with VLA‐4 activation, eventually decreasing soluble VCAM‐1 binding and reducing downstream ERK phosphorylation of blood‐residing CLL cells [127]. Here, VCAM1 is linked to B-cell chronic lymphocytic leukemia.