During the development of sepsis, Tregs subdue inflammation and tissue damage, and they may also cause immune dysfunction, such as induction of T-lymphocytic apoptosis, inhibition of CD4+/CD8+ T-lymphocytic function, and mediation of shifting from the helper T cell 1 (Th1) to Th2 response, especially immunoparalysis via expression of CTLA-4 and TGF-βm+, as well as anti-inflammatory cytokines (IL-10 and TGF-β) [12–17]. The gene discussed is CTLA4; the disease is Sepsis.