Collectively, ibrutinib and acalabrutinib specifically inhibit GPVI-mediated platelet activation and aggregation via BTK/TEC-dependent mechanisms and also affect αIIbβ3- and GPIb-IX-mediated signaling in platelets by inhibiting the SYK-PI3K-BTK axis (Table 5), which contribute to the increased bleeding observed in CLL and MCL patients. The gene discussed is BTK; the disease is B-cell chronic lymphocytic leukemia.