Next, we employed three mouse AML models including one granulocytic M2b subtype expressing a human AML1-ETO9a (AE9a) fusion protein and one granulocytic M3/APL subtype expressing PML-RARα (PR) fusion protein as well as one monocytic M5 subtype expressing MLL-AF9 (MF9) fusion protein to test whether JMJD3 possessed a genuine oncorepressor potential in AML23–25. The gene discussed is KMT2A; the disease is acute myeloid leukemia.