In the recent study involving CLL cells,30 the ability of MCL-1 antagonists to induce MCL-1 stabilization was linked to multiple factors, including de-ubiquitination, destabilization of the Mule E3-ligase, and dissociation of MCL-1/NOXA interactions.30 Here, we found that in AML cells exposed to MCL-1 antagonists/SKI-606 exhibited a marked increase in the association of MCL-1 and K48 ubiquitination, a known degradative process.47 The mechanism by which Src interruption promotes degradative ubiquitination of MCL-1 remains to be defined. This evidence concerns the gene MCL1 and B-cell chronic lymphocytic leukemia.