Using this novel ETP leukemia mouse model to explore potential therapeutic strategies for this chemotherapy-resistant cancer, we found that inactivation of Ezh2 in DKOITD bone marrow drives upregulation of gene expression via loss of H3K27me3 and gain of H3K27ac, as expected given the role of EZH2 as part of the polycomb repressive complex 2 (PRC2) [6]. This evidence concerns the gene EZH2 and leukemia.