When the Tim-3 pathway was decreased and/or blocked in sepsis by an antagonist monoclonal antibody against Tim-3 and/or soluble Tim-3 protein, the levels of Th1- and Th17-related cytokines (IFN-γ, IL-17, IL-2, and IL-6) increased, and the immunosuppressive function of Treg cells significantly decreased [24]; furthermore, the expression of the cytokine IL-10 also significantly decreased, suggesting that Tim-3 plays important roles in maintaining homeostasis in sepsis in both humans and a mouse model [22,23]. This evidence concerns the gene IL2 and Sepsis.