Experiments in mice in which toll-like receptor 4 was specifically deleted from hepatocytes, i.e., parenchymal liver cells, demonstrated that toll-like receptor 4 expression in hepatocytes is critical for the clearance of lipopolysaccharide, both in a model of polymicrobial sepsis induced by caecal ligation and puncture and in a model of endotoxemia [42]. This evidence concerns the gene TLR4 and Sepsis.