Consistent with this, unsupervised hierarchical clustering of differentially expressed genes amongst AML patients with the AML1-ETO translocation revealed that ASXL2-mutant AML1-ETO samples form a distinct transcriptional subset of AML1-ETO AML, an effect not seen with other common genetic alterations in AML1-ETO AML (Fig. 5a). This evidence concerns the gene ASXL2 and acute myeloid leukemia.