An early study on acute lung injury (ALI) as well as studies utilizing intraperitoneal (IP) LPS injections in gain-of-function models of transgenic mice with human SR-BI (hSR-BI) and hSR-BII expression revealed that both receptors mediate LPS uptake and contribute to LPS-induced inflammatory signaling and tissue injury, including the liver and kidney [12], thus supporting a potentially detrimental role of these receptors during IP-induced endotoxemia and LPS interaction with the liver and kidney reticular endothelial system (RES) [23]. The gene discussed is SCARB1; the disease is serum lipopolysaccharide activity.