Initial studies on a primate sepsis model by Escherichia coli infusion, revealed that administration of a C5a inhibitor resulted in prevention of mortality, amelioration of ARDS and acceleration of recovery [46] while a subsequent study on the same animal model with a C5a inhibitor administration confirmed the reduction of mortality and pulmonary edema, as well as the reduction of C5a levels in the treated animals, indicating the important role of C5a in ARDS development and progression [47]. The gene discussed is C5AR1; the disease is acute respiratory distress syndrome.