A chromatin-mediated change in the alternative splicing of these H3K79me2-marked exons, by knocking-down the H3K79 methyltransferase Dot1L, significantly reduced cell proliferation and tumour progression in two of these leukaemia cancer cell lines, highlighting the coordinated regulation of cancer-related splicing events by H3K79me235. The gene discussed is DOT1L; the disease is cancer.