CD34+CD38−CD32+ and CD34+CD38−CD25+ LSCs could initiate AML development in NSG mice, were cell cycle-quiescent and chemotherapy-resistant in vivo and expressed the transcription factor WT1 and the kinase HCK. CD32 and CD25 could thus represent valuable targets for LSC-directed therapy, as suggested by the maintenance of long-term multi-lineage hematopoietic reconstitution capacity by normal human HSCs depleted of CD32/CD25-expressing cells. This evidence concerns the gene WT1 and acute myeloid leukemia.