For example, because MLLr proteins recruit the histone methyltransferase DOT1L to the HOXA locus promoting hyper-methylation at histone H3 lysine 79 and subsequent high HOXA9 transcription (Krivtsov et al., 2008), selective DOT1L inhibitors have been exploited to inhibit leukemia development and HOXA9 expression in MLLr leukemias and are now in clinical trials (Chen et al., 2015; Stein and Tallman, 2015). This evidence concerns the gene PRDM9 and leukemia.