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BRD 4 is a  BET  family protein that binds acetylated histones and regulates transcription.  BET / BRD 4 inhibitors block blood cancer growth and inflammation and serve as a new therapeutic strategy. However, the biological role of  BRD 4 in normal hematopoiesis and inflammation is not fully understood. Analysis of Brd4 conditional knockout ( KO ) mice showed that  BRD 4 is required for hematopoietic stem cell expansion and progenitor development. Nevertheless,  BRD 4 played limited roles in macrophage development and inflammatory response to  LPS . Ch IP ‐seq analysis showed that despite its limited importance,  BRD 4 broadly occupied the macrophage genome and participated in super‐enhancer ( SE ) formation. Although  BRD 4 is critical for  SE  formation in cancer,  BRD 4 was not required for macrophage  SE s, as  KO  macrophages created alternate,  BRD 4‐less  SE s that compensated  BRD 4 loss. This and additional mechanisms led to the retention of inflammatory responses in macrophages. Our results illustrate a context‐dependent role of  BRD 4 and plasticity of epigenetic regulation.

BRD4 directs hematopoietic stem cell development and modulates macrophage inflammatory responses