Although Evi1 could not enrich MLL-ENL AML LSCs in our model, it is possible that Evi1 reduction in the bulk leukemia cells would be a key in amelioration of MLL-related leukemia as previously investigated.25 Exact introduction of these oncogenes to HSCs by different approaches such as via a transgene or a knocking-in technology could unravel the relation between AML stem cells and Evi1. The gene discussed is MECOM; the disease is acute myeloid leukemia.