To evaluate the role of Ezh2 in AML maintenance in vivo, and therefore determine the therapeutic implications of targeting EZH2 in established AML, we then generated primary MLL-AF9 and AML1-ETO9a murine leukemias on an Ezh2fl/fl;Mx1-Cre background but did not treat donor or recipient mice with poly(I)-poly(C) (pIpC), thus leaving the Ezh2 locus intact (Fig. 1 d). This evidence concerns the gene RUNX1 and acute myeloid leukemia.