Consistent with these findings, Sharp1 mRNA was elevated in MLL-AF6 AML cells compared to BM Granulocyte-Macrophage Progenitor (GMP) and granulocytes, which are the phenotypic normal hematopoietic counterparts for AML cells15, while the expression in MLL-AF9 AML was comparable to normal BM GMP and higher than granulocytes (Supplementary Fig. 4e), suggesting that upregulated Sharp1 may confer oncogenic properties to murine MLL-AF6 AML, but not to MLL-AF9 AML. The gene discussed is KMT2A; the disease is acute myeloid leukemia.