During the development of sepsis, Tregs can mainly inhibit the activation of CD4+ T cells through various mechanisms, mainly including the pathway of cellular contact (e.g., CTLA-4 and TGF-βm+) and inhibitory cytokines (e.g., IL-10 and TGF-β), as well as upregulating the antiapoptotic ability of Tregs [11–15, 23, 24]. The gene discussed is IL10; the disease is Sepsis.