In contrast to other Evi1-transgenic mouse models that developed AML (13, 21), our model demonstrated that EVI1 overexpression leads to the development of MDS/MPN–like disease, characterized by dysregulated hematopoiesis, anemia, thrombocytopenia, and expansion of myeloid progenitor cells, which is consistent with the phenotypes being observed in EVI1hi MDS and MDS/MPN patients due to inv(3)/t(3;3) rearrangements (17). The gene discussed is MECOM; the disease is myelodysplastic syndrome.