In all, these results support the model in which the core regulatory circuitry of AML cells is organized aberrantly by MYB and its associated co-factors including LYL1, C/EBP family members, E2A, SATB1 and LMO2, which co-operate in the induction and maintenance of oncogenic gene expression, as presumably co-opted by distinct oncogenes in biologically diverse subtypes of AML (Figure 13). This evidence concerns the gene LMO2 and acute myeloid leukemia.