KMT2A and acute myeloid leukemia: Here, we used MSC-specific inducible Mettl3 knockout mice Prrx1-CreERT2;Mettl3fl/fl and an MLL-AF9 AML mouse model to define the influence of Mettl3 deficiency on AML progression, response to chemotherapy in vivo, and the underlying cellular and molecular pathways.