The exact mechanism by which Hotairm1 promotes late sepsis is unclear, but we predict that Hotairm1-driven and nuclear S100A9 acts as a transcription co-factor to induce expression of immunosuppressive genes in Gr1+CD11b+ myeloid precursors, thus contributing to the MDSC development and late sepsis phenotype. This evidence concerns the gene S100A9 and Sepsis.