These findings are significant because we have previouslyshown that Hotairm1 induces S100A9 proteindephosphorylation and accumulation in the nucleus in MDSCs during late sepsis [20,22].While the current study does not provide mechanistic detail on howS100A9 regulates IL-10 and TGF-β promoters in MDSCs(e.g., if S100A9 interacts with transcription co-factors), ourresults demonstrate that assembly of S100A9 protein at IL-10 andTGF-β promoters is sufficient to activate their transcription. This evidence concerns the gene TGFB1 and Sepsis.