Given that expression of the AML1-ETO fusion is not sufficient to generate overt AML on its own20, 21, 22, 23, 24, the unique enrichment of ASXL2 mutations in this subset of AML suggests that ASXL2 mutations may be an important cooperating genetic alteration in the pathogenesis of AML1-ETO AML. Here, RUNX1T1 is linked to acute myeloid leukemia.