However, it does not reflect what is observed with more common forms of AML such as those associated with RUNX1-RUNX1T1 (AML1-ETO), where progression in mouse models is slow and infrequent (7, 16), or clonal hematopoiesis, in which the associated mutations (e.g., in IDH1/2, TET2, DNMT3A) convey a self-renewal advantage but require additional genetic events for leukemia (7, 16). Here, RUNX1T1 is linked to leukemia.