In parallel, Brunetti et al. demonstrated that HOXA (and HOXB) genes are not only direct downstream targets of NPM1c+ protein but also that the interaction between exportin-1 (XPO-1), a nuclear pore exporter, and NPM1c+ protein, maintains mutated-NPM1 in the cytoplasmic compartment as an important point explaining AML occurrence [78]. This evidence concerns the gene XPO1 and acute myeloid leukemia.