With sepsis, Tregs subdued the process of inflammation and tissue damage while also causing immune dysfunction, including 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 via the expression of CTLA-4 and TGF-βm+, as well as anti-inflammatory cytokines (IL-10 and TGF-β) [10–15]. This evidence concerns the gene CTLA4 and Sepsis.