Several subsets, ranging from the common NPM1 mutation (~33% of AML) to the rarer lysine methyltransferase 2A (KMT2A) (5–10% of AML) rearrangements (formerly known as mixed lineage leukemia, MLL), may have a common sensitivity to disruption of the protein menin as these two subsets share a common, targetable final pathway. This evidence concerns the gene NPM1 and acute myeloid leukemia.