Furthermore, both toll-like receptor 4 (TLR4), an immune receptor, and intercellular adhesion molecule 1 (ICAM-1) respond to lipopolysaccharide binding, but reducing PMN counts increases thrombosis and increases plasminogen activator inhibitor-1 (PAI-1), increases circulating Factor XIII, and decreases uPA observed in endotoxemia [71]. The gene discussed is ICAM1; the disease is serum lipopolysaccharide activity.