TO THE EDITOR:

Chromosomal rearrangements involving the mixed lineage leukemia gene (MLL1, KMT2A) define a genetically distinct subset of acute myelogenous leukemias (AMLs) and acute lymphoblastic leukemias.1-4 MLL rearrangements encode an MLL fusion protein that drives leukemia development. Direct targeting of the MLL fusions is not yet feasible, but targeting members of the oncogenic MLL fusion complex is showing promise. This is exemplified by the development of Menin-MLL1 interaction inhibitors that disrupt the integrity of the oncogenic MLL fusion protein complex5-8  as well as enzymatic inhibitors of the histone methyltransferase DOT1L.9,10  Both Menin and DOT1L have been shown to be essential for maintenance of MLL fusion–driven oncogenic gene expression in human and murine model systems.5,6,11-15  Menin inhibitors are orally bioavailable, exhibit favorable pharmacokinetics, and show potent antileukemic properties in vivo.5,8  Therefore, 2 different...

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