Recent studies, including those from our laboratory, indicate that SR-BI protects against sepsis through multiple mechanisms: (1) preventing nitric oxide-induced cytotoxicity; (2) promoting hepatic lipopolysaccharide (LPS) clearance and regulating cholesterol metabolism in the liver; (3) inhibiting LPS-induced inflammatory signaling in macrophages; and (4) mediating the uptake of cholesterol from HDL for inducible glucocorticoid (iGC) synthesis in the adrenal gland, which controls systemic inflammatory response. This evidence concerns the gene SCARB1 and Sepsis.