Finally, the pharmacological profiling of residual circulating CLL cells from patients being treated with the BTK inhibitor ibrutinib revealed an exquisite dependence on BCL2 and sensitivity to venetoclax, which is likely related to increased mobilization of lymphocytes from lymph nodes and decreased levels of MCL1 and BCLxL following ibrutinib therapy [64]. This evidence concerns the gene BCL2L1 and B-cell chronic lymphocytic leukemia.