Given the prevalence of MEIS1 overexpression in AML,31, 32, 33, 34 its critical role in MN1 leukemic transformation,10 and its upregulated gene expression in the two MN1 leukemic versus non-leukemic data sets examined (MN1 versus MN1Δ1 and cKit versus CD11b),14 the minimal effects of Meis1 knockdown on growth, self-renewal, and impairment of differentiation stimulated closer examination of a possible role for the MEIS family member MEIS2. This evidence concerns the gene KIT and acute myeloid leukemia.