In this regard, accumulating evidence suggests that the cyclooxygenase-2 (COX-2)/PGE2 pathway plays an important role in augmenting inflammatory immune response in sepsis-associated ARDS, since the inhibition of lung PGE2 production inhibits oedema, neutrophil infiltration, proinflammatory cytokine production, adhesion molecules expression, and restored lung morphology, increasing survival in polymicrobial sepsis [54]. The gene discussed is PTGS2; the disease is acute respiratory distress syndrome.