Epigenetic activation or inactivation of genes plays a critical role in many important human diseases, especially in cancer. A major mechanism for epigenetic inactivation of the genes is methylation of CpG islands in genome DNA caused by DNA methyltransferases. Histone methyltransferases (HMTs) control or regulate DNA methylation through chromatin-dependent transcription repression or activation. HMTs transfer 1-3 methyl groups from S-adenosyl-L-methionine to the lysine and arginine residues of histone proteins. Dot1 is a histone methyltransferase that catalyzes methylation of histone H3 at lysine 79 (H3-K79) in mammalian cells.Intergenic H3-K79 mono-methylation is a mark of enhancer regions and may provide unique binding surfaces along the chromatin fiber to stabilize interactions between enhancers and their target promoters. The H3-K79 mono-methylation can be changed by inhibition or activation of HMTs. Thus quantitative detection of mono-methyl histone H3-K79 would provide useful in
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