With the development of sepsis, Tregs subdue inflammation and tissue damage, while they could 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 (Th) 1 to Th 2 response, especially immunoparalysis via expression of CTLA-4 and membrane associated transforming growth factor-β (TGF-βm+), as well as anti-inflammatory cytokines (IL-10 and TGF-β) [12–17]. This evidence concerns the gene CTLA4 and Sepsis.