KMT2A and acute myeloid leukemia: Increases in MCL-1 gene copy number and concomitantly elevated MCL-1 protein are found in a substantial fraction of diverse cancer types.31 For a few cell lines derived from such cancers, MCL-1 knockdown by RNA interference was shown to cause apoptosis, demonstrating that MCL-1 is critical for their sustained survival.31 Similarly, acute myeloid leukemia (AML) cells driven by enforced expression of c-MYC or the MLL-ENL and MLL-AF9 fusion onco-proteins and c-MYC- or BCR-ABL-driven pre-B/B lymphomas were rapidly killed upon inducible genetic deletion or blockade of MCL-1.32, 33, 34, 35