Accumulative evidence has shown that a combination of Foxp-3, CTLA-4, membrane-associated TGF-β, and inhibitory cytokines (IL-10 and TGF-β) might serve as active markers for Tregs in sepsis, and it appeared to be involved in the immunosuppressive ability of Tregs on CD4+ T lymphocytes, including apoptosis, a shift to anti-inflammatory cytokines, and anergy43, 44. Here, FOXP3 is linked to Sepsis.