MYELOID BIOLOGY: Edited by David C. DaleThe role of the transcriptional repressor growth factor independent 1 in the formation of myeloid cellsFraszczak, Jennifera,b; Möröy, Tarika,b,cAuthor Information aInstitut de recherches cliniques de Montréal (IRCM) bDépartement de microbiologie, infectiologie et immunologie, Université de Montréal cDivision of Experimental Medicine, McGill University, Montréal, Québec, Canada Correspondence to Dr Tarik Möröy, Institut de recherches cliniques de Montréal (IRCM), 110 avenue des Pins Ouest, Montréal, Québec, Canada H2W 1R7. Tel: +1 514 987 5501; fax: +1 514 987 5679; e-mail: [email protected] Current Opinion in Hematology: January 2017 - Volume 24 - Issue 1 - p 32-37 doi: 10.1097/MOH.0000000000000295 Buy Metrics Abstract Purpose of review Growth factor independent 1 (Gfi1) is a transcriptional repressor that plays multiple roles during myeloid commitment and development. Gfi1-deficient mice lack granulocytes, accumulate aberrant monocytes and show a hyperactivity of macrophages toward bacterial cell wall components. Since these initial findings, numerous additional studies have confirmed the role of Gfi1 in myeloid differentiation from hematopoietic stem cells and multipotent progenitors to bipotential lymphoid/myeloid precursors and myeloid effector cells. This review will summarize the existing knowledge concerning the mechanisms through which Gfi1 exerts these actions and will highlight recent insights into its additional implication in myeloid malignancies. Recent findings Gfi1 has more recently been implicated in myeloid malignancies, in particular in myelodysplasia, myeloproliferative neoplasms and in acute myeloid leukemia, a fatal disease, which is essentially treated today the same way as 30 years ago. Summary Recent findings on the role of Gfi1 in myeloid malignancies together with the knowledge base built over many years on this molecule may help us to find new ways to predict the progression of acute myeloid leukemia and to design more efficient epigenetic drugs to treat this disease. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.