ASXL1 and chronic myelomonocytic leukemia: Importantly, underscoring the potential of BET bromodomain inhibition, Binder et al. recently demonstrated that leukemogenic gene activation (e.g., mitotic kinases, HOXA cluster genes, MAPKand receptor tyrosine kinase signaling) in samples from CMML patients with truncating ASXL1 mutations were associated with permissive promoter chromatin states due to H3K27ac and H34me1 deposition, and ASXL1 mutation-specific de novo accessibility of distal enhancers binding ETS transcription factors, as well as BRD4 [129].