found that by introducing a KRAS mutation and then KMT2A-ENL rearrangement in bone marrow multipotent granulocyte-monocyte-lymphoid progenitors (GMLPs), mice would develop T-ALL (27), which supports the hypothesis of a cellular origin of ETP-ALL from bone marrow multipotent progenitors. The gene discussed is MLLT1; the disease is acute lymphoblastic leukemia.