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Epigenetic changes can contribute to development of acute myeloid leukemia (AML), a malignant disease of the bone marrow. A single-nucleotide polymorphism of transcription factor growth factor independence 1 (GFI1) generates a protein with an asparagine at position 36 (GFI1 36N ) instead of a serine at position 36 (GFI1 36S ), which is associated with de novo AML in humans. However, how GFI1 36N predisposes to AML is poorly understood. To explore the mechanism, we used knock-in mouse strainsdoi:10.1016/j.exphem.2016.05.004 pmid:27216773 fatcat:yieut24znrg3zkudmjq5hcd3vm