Exportin-1 (XPO1/CRM1), a key nuclear export receptor, mediates pathologic crosstalk between AML blasts and the bone-marrow niche in NPM1-mutant AML: the frameshift mutation in NPM1 (NPM1c) generates a strong leucine-rich nuclear export signal (NES), driving cytoplasmic mislocalization of NPM1. This evidence concerns the gene NPM1 and acute myeloid leukemia.