It was shown that high MCL-1 expression and BCL-2 phosphorylation markedly reduced the ability of ABT-737 to induce apoptosis [16], whereas up-regulation of MCL-1 and BCL-XL was found to be responsible for the resistance of myeloid leukemia cell lines to ABT-199 [19]. This evidence concerns the gene MCL1 and myeloid leukemia.