Although EVI1 has been reported to transcriptionally repress or suppress TGFb signaling by recruiting Smad3 and the co-repressor CtBP [8]–[10], we showed that EVI1 is directly associated with the GATA-2 promoter and upregulates GATA-2 transcription to maintain hematopoietic stem cells (HSCs) and AML with EVI1high expression [11], [12] in EVI1-deficient mice. The gene discussed is GATA2; the disease is acute myeloid leukemia.