The critical role of CD14 in the regulation of LPS-induced inflammation was evidenced by: (1) an enhanced sensitivity to lethal endotoxemia in CD14-over-expressing mice [19]; (2) a reduced susceptibility to lethal endotoxemia in CD14-deficient mice [20]; and (3) an abolishment of LPS-induced production of early cytokines (e.g., TNF) in CD14-deficient innate immune cells [21,22]. This evidence concerns the gene CD14 and serum lipopolysaccharide activity.