The presence of the AML1-ETO fusion protein in HSCs alone does not cause leukemia, as secondary genetic lesions ((like ICSBP deficiency [27], mutation in FLT3 [28] and C-KIT [29]) and/or potential leukemia supporting niche-effects are necessary for the progression to AML. The gene discussed is RUNX1T1; the disease is acute myeloid leukemia.