Also consistent with our hypothesis are the findings that survival in mouse models of sepsis can be improved by infusion of soluble CD52 (61), and that the sialic acid-binding feature of HMGB1 is restricted to the disulfide form of HMGB1 (26), which is expected to be formed when the cytosolic reduced form is released into the oxidizing environment of the bloodstream. The gene discussed is HMGB1; the disease is Sepsis.