It is thus plausible that IFN-γ, a proinflammatory cytokine predominantly derived from spleen [46], contributes to lethal endotoxemia [47], [48] or sepsis [49] partly by stimulating HMGB1 release [50] and partly by inhibiting hepatic fetuin-A expression. The gene discussed is IFNG; the disease is serum lipopolysaccharide activity.