Interestingly, and along the same lines, de Rooij and colleagues recently reported that the BTK inhibitor ibrutinib strongly inhibits VLA4 integrin-mediated adhesion of lymphoma cell lines and primary CLL cells to fibronectin and VCAM-1, and proposed this activity, along with inhibition of chemokine receptor function, as an underlying mechanism to explain the CLL cell redistribution caused by this BTK inhibitor [40]. The gene discussed is VCAM1; the disease is lymphoma.