Approaches to down-regulate MCL-1 expression have been directed multiple ways: inhibiting its transcription via CDK9 inhibition, as is the case with alvocidib and other CDK inhibitors [113, 114]; at the translational level, as occurring in human leukemia cells exposed to sorafenib [171]; or by targeting protein-protein interactions to directly affect MCL-1 anti-apoptotic activity [8, 172–174]. This evidence concerns the gene MCL1 and leukemia.