We used a chronic model of sepsis in mice to showthat S100A9 release from MDSCs and circulating phagocytes decreases after earlysepsis and that targeting the S100a9 gene improves survival.Surprisingly, we find that intracellular S100A9 protein translocates from the cytosolto nucleus in Gr1+CD11b+ MDSCs during latesepsis and promotes expression of miR-21 and miR-181b immune repressor mediators. The gene discussed is ITGAM; the disease is Sepsis.