Similarly, we validated the finding that MCL-1 and BCL-XL up-regulation can drive resistance to the potential to be used to address many other questions in selective BCL-2 inhibitor ABT-199 (venetoclax) in acute myeloid leukemia (AML) by demonstrating the resensitization of cells with acquired resistance through knockdown or small molecule inhibition of these candidate resistance proteins [48]. The gene discussed is MCL1; the disease is acute myeloid leukemia.