Resistance mechanisms observed in CLL patients treated with venetoclax include the acquisition of BCL-2 mutations such as the Gly101Val mutation that reduce venetoclax binding to BCL-2, or compensatory overexpression of other pro-survival proteins BCL-xL and MCL-1 [65,66,67,68,69,70]. The gene discussed is BCL2; the disease is B-cell chronic lymphocytic leukemia.