In the development of sepsis, Tregs can mainly inhibit the activation of T-lymphocytes, especially CD4+ T-lymphocytes through various suppressive mechanisms, including inhibitory cytokines (such as IL-10 and TGF-β) and cell-to-cell contact (such as CTLA-4 and TGF-βm+), inhibition of cytolysis (especially granzymes), downregulation of metabolic disruption, and suppression of maturation and function of antigen presenting cells, as well as upregulation of antiapoptotic ability [12, 14–17]. This evidence concerns the gene CD4 and Sepsis.