The DOT1L inhibitor efficiency on mutated-NPM1 might partially be explained by an increase in the level of DOT1L protein (but not mRNA) in mutated-NPM AML [75] and by the presence of both DOT1L and NPM1 proteins within a proteic complex as identified by tandem affinity purification and mass spectrometry analysis [137]. This evidence concerns the gene DOT1L and acute myeloid leukemia.