Next to study leukemogenesis mediated by AML1-ETO and ASXL2 loss in the genetic configuration most representative of human AML, we crossed mice bearing expression of the Aml1-Eto fusion from the endogenous locus of Aml1 (Aml1-Eto conditional knockin mice23) to Mx1-cre Asxl2fl/fl mice to generate Mx1-cre Aml1-Eto Asxl2fl/WT and Mx1-cre Aml1-Eto Asxl2 WT mice (Supplementary Fig. 9a–c). Here, ASXL2 is linked to acute myeloid leukemia.