AVA and its existing analogs may thus represent a novel therapeutic strategy capable of targeting defined subsets of AML patients through their ability to interact with both NPM1 and CRM1, and possibly leukemia inititation cells as recently demonstrated for selinexor (KPT-330).54 We believe that further exploration of this family of compounds will lead to the identification of candidate molecules with improved physicochemical and PK properties for further evaluation in preclinical contexts. Here, NPM1 is linked to acute myeloid leukemia.