Indeed, the various functional assays in this study confirmed that such exon skipping events were highly coordinated by the H3K79me2 or DOT1L activities with DOT1L siRNA treatment in two MLL-r AML cell lines (Fig. 5), providing a new line of evidence of a co-transcriptional splicing process involved in AML. The gene discussed is KMT2A; the disease is acute myeloid leukemia.