Many studies have suggested that the aberrant in vivo expression of TF plays a pivotal role in sepsis-associated blood clotting change, as indicated by the following observations: 1) the impairment of the TF pathway by various means prevents coagulation abnormalities and lethality in animal models of sepsis or endotoxemia [9–11]; 2) the plasma levels of TF are increased in septic patients and generally associated with raised concentrations of markers of clotting activation [9, 11, 12]. The gene discussed is TF; the disease is serum lipopolysaccharide activity.