Using a sepsis model, engagement of Toll-like receptor 4 (TLR4) on endothelial cells via lipopolysaccharide (LPS) produces excessive IL-6, which in turn interacts with sIL-6R and gp130 to create a positive feedback loop of more IL-6 production as well as a variety of other proinflammatory molecules, such as plasminogen activator inhibitor 1 (PAI-1) (53). This evidence concerns the gene SERPINE1 and Sepsis.