Nucleophosmin　(NPM1　or　B23.1)　is　a　ubiquitously　expressed　nuclear　phosphoprotein　that　plays　key　role　in　several　cellular　processes,　including　ribosome　biogenesis,　centrosome　duplication,　cell　cycle　progression,　cell　growth,　and　transformation.　NPM1　is　one　of　the　most　frequently　mutated　genes　in　AML.　EDAG　is　a　hematopoietic　tissue-specific　transcription　regulator　that　plays　a　key　role　in　maintaining　the　homeostasis　of　hematopoietic　lineage　commitment.　In　AML　patients,　the　high　expression-　level　of　EDAG　is　associated　with　poor　prognosis.　Our　previous　study　suggest　that　EDAG　is　a　physiological　binding　partner　of　NPM1　and　regulates　NPM1　protein　stability,　however,　whether　EDAG　regulates　NPM1　in　AML　patients　and　whether　EDAG　regulates　NPM1　mutations　remain　unknown.　In　the　present　study,　we　found　that　in　bone　marrow　CD34(+)　cells　from　AML　patients,　silencing　of　EDAG　led　to　decreased　protein　stability　of　NPM1　protein　and　increased　cell　sensitivity　to　daunorubicin.　Although　EDAG　failed　to　interact　with　NPMc(+)　and　regulate　its　protein　stability　in　normal　culture　condition,　with　leptomycin　B　treatment,　EDAG　overexpression　enhanced　the　protein　stability　of　NPMc(+).　In　AML　patients　with　NPMc(+),　the　CD34(+)　cells　were　more　responsive　to　daunorubicin　treatment　than　the　cells　from　AML　with　wild　type　NPM1,　and　silencing　of　EDAG　weakly　increased　the　sensitivity　to　daunorubicin.　These　results　suggested　a　potential　role　of　EDAG　in　chemotherapy　of　AML　and　the　＂escape＂　of　NPMc(+)　protein　from　EDAG　stabilization　might　contribute　to　the　favorable　prognosis　of　AML　with　NPMc(+)