Studies using APOE deficient mice confirmed the role of APOE in host susceptibility to endotoxemia and Klebsiella pneumoniae infection [14], while transgenic mice expressing human APOE3 and APOE4 genes revealed an isoform-specific effect of APOE on the proinflammatory response to lipopolysaccharide [31]. This evidence concerns the gene APOE and serum lipopolysaccharide activity.