Therefore, we could not find evidence for the concept that rh-APC ameliorates endothelial barrier dysfunction and increased permeability and thereby attenuates the course of ARDS in man, as suggested by preclinical studies via a cytoprotective effect involving PAR-1 and S1P pathways, irrespective of anti-inflammatory effects [11], [14], [15]. The gene discussed is F2R; the disease is acute respiratory distress syndrome.