Among most of leukemogenic fusion proteins the aberrant localization that the translocation partners are forced in when compared to their wt counterparts contributes to leukemogenesis most likely by a sequester of interaction partners. The aim was to disclose the role of localization of DEK/NUP214 and the related sequester of proteins interacting with DEK/NUP214 for the induction t(6;9)- AML. The pathways indispensable for the induction of the leukemogenic phenotype were worked out by comparing the interactome of the full-length fusion protein to that of biologiaclly-dead mutants.