Since a similar H3K4 hypertrimethylation defect was noted in mouse MLL1-AF10 LSCs (with AF designating the fusion partner) (19) and in patient-derived MLL1-AF4 blast cells (37), these results suggested that the enzymatic activity of MLL1 may be required to limit the spread of the gene-activating H3K4 trimethyl mark. This evidence concerns the gene KMT2A and atrial fibrillation.