These results show that TsES protected mice from polymicrobial sepsis via MR activation, which could engage in crosstalk with TLR signaling to inhibit MyD88 and NF-κB. Ligand binding to MR may have an immunosuppressive function characterized by a profile of anti-inflammatory cytokines, which could prevent the generation of Th1-polarized responses [36], although, in other infection models like Candida albicans, MR can lead to increase inflammatory cytokines production and Th17 immune responses [37, 38]. The gene discussed is NR3C2; the disease is Sepsis.