DOT1L and nasopharyngeal carcinoma: To investigate the cell-type-specific causal contribution of DOT1L enzymatic function for the genome-wide transcriptional activity and for the overall epigenetic context, we inhibited the enzyme in mESC and NPC by treating cells for 48 h with the S-adenosyl methionine (SAM) competitor Pinometostat (EPZ5676, EPZ).