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Acute myeloid leukaemia (AML) is an aggressive blood cancer characterized by the unregulated proliferation of immature myeloblasts. Gene mutations have been shown to have a large effect on pathogenesis, inter-tumour heterogeneity and clinical outcomes in AML1, 2, 3, 4, 5, 6, 7–8; however, the role of epigenetic alterations in these respects has been investigated less extensively. Here we use ATAC-
