Consecutive studies by Gazzar et al. [62, 63] showed that intracellular S100A9 enhanced assembly of signal transducer and activator of transcription 3-CCAAT/enhancer-binding protein alpha in an IL-10 dependent manner, which in turn upregulated expression of immune repressor mediators including microRNA-21 and microRNA-181b, thereby facilitating expansion and immunosuppression of MDSCs during late sepsis. The gene discussed is S100A9; the disease is Sepsis.