This finding strongly contrasts with previous studies that have shown that increased levels of MCL-1, as well as an increased apoptotic dependency to MCL-1, have been described as the main driver mechanisms of venetoclax resistance in CLL [25,27], diffuse large B-cell lymphoma [24,28], multiple myeloma [12,29], and acute myeloid leukemia [11,26]. The gene discussed is MCL1; the disease is B-cell chronic lymphocytic leukemia.