NUP98 and acute myeloid leukemia: Since DOT1L is a highly selective regulator of the AML oncotranscriptome in several AML subtypes, such as KMT2A, MLLT10 or NUP98-rearranged AML, as well as of NPM1 mutant AML, further investigation of DOT1L inhibition with better pharmacological properties (85, 87) is warranted.