Mechanistically, the MLL1 fusion protein in acute myeloid leukemia (AML) causes abnormal recruitment of histone modification enzymes, including DOT1L (KMT4) and protein arginine methyltransferase (PRMT) 1, at target genes for epigenetic reprogramming, conferring stem cell-like properties67,68. This evidence concerns the gene DOT1L and acute myeloid leukemia.