Evi-1hasbeenrecognizedasoneofthedominantoncogenesassociatedwithmurineandhumanmyeloidleukemia.Here,weshowthathematopoieticstemcells（HSCs）inEvi-1-deficientembryosareseverelyreducedinnumberwithdefectiveproliferativeandrepopulatingcapacity.SelectiveablationofEvi-1inTie2+cellsmimicsEvi-1deficiency,suggestingthatEvi-1functionisrequiredinTie2+hematopoieticstem/progenitors.ConditionaldeletionofEvi-1intheadulthematopoieticsystemrevealedthatEvi-1-deficientbonemarrowHSCscannotmaintainhematopoiesisandlosetheirrepopulatingability.Incontrast,Evi-1isdispensableforbloodcelllineagecommitment.Evi-1+/−miceexhibittheintermediatephenotypeforHSCactivity,suggestingagenedosagerequirementforEvi-1.WefurtherdemonstratethatdisruptionofEvi-1intransformedleukemiccellsleadstosignificantlossoftheirproliferativeactivitybothinvitroandinvivo.Thus,Evi-1isacommonandcriticalregulatoressentialforproliferationofembryonic/adultHSCsandtransformedleukemiccells.
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