The high responses and durable remissions observed with ibrutinib in MCL, WM, and CLL are believed to be influenced by the binding properties of ibrutinib; ibrutinib covalently and irreversibly attaches to C481 in the active site of the BTK protein, thereby effectively inhibiting kinase activity until new BTK protein is generated. This evidence concerns the gene BTK and B-cell chronic lymphocytic leukemia.