Although originally LBP was recognized as a key factor triggering the inflammatory response to microbial assault [28], further analyses using animal models of sepsis demonstrated that exogenously administrated recombinant LBP is able to decrease LPS-induced cytokine release and improve the clinical outcomes of intraperitoneally infected animals [29,30], which could be explained by LBP acting as bacterial phagocytosis enhancer [31,32]. The gene discussed is LBP; the disease is Sepsis.