The current model for the contribution of EVI1 misexpression and Gata2 haploinsufficiency to leukemogenesis. Although EVI1 misexpression promotes expansion of the B220⁺Gr1^–c-Kit⁺ leukemic progenitors, GATA2 abundance contributes to fate determination of the EVI1-expressing leukemic cells. The B220⁺Gr1^–c-Kit⁺ cells that express high GATA2 exhibit a GMP-like phenotype and differentiate into Gr1⁺ myeloid leukemic cells (upper arrow). In contrast, when Gata2 expression levels in the B220⁺Gr1^–c-Kit⁺ population are diminished, because of either Gata2 heterozygous deletion or spontaneous (unknown) mutations, the B220⁺Gr1^–c-Kit⁺ cells fail to differentiate into the myeloid lineage and acquire B-lymphoid–primed (lymphoid-primed multipotent progenitor [LMPP] to pre-pro B-like) characteristics (lower arrow). Furthermore, Gata2 reduction enhances expansion of the leukemic cells, which results in a more aggressive leukemia.