The tumor-suppressive function of the ASXL1-BAP1 axis was further highlighted by Cao et al. These investigators demonstrated that Asxl1 loss enabled IL-3 independent growth in an AML cell line (murine 32D cells) due to the increased activation of AKT resulting from the increased levels of H2AK119Ub1 (globally as well) and H3K27me3 at the Pten promoter, which maintained Pten silencing (PTEN negatively regulates the PI3K-AKT pathway). The gene discussed is ASXL1; the disease is neoplasm.