To answer this question, we established an in vitro as well as an in vivo lipopolysaccharide (LPS)-induced sepsis-associated ALI model, specifically examined the biological effects of pre-treating cells with LXA4 receptor agonist, BML-111 on the apoptosis and autophagy of AMs, explored the underlying signaling mechanisms, and assessed the prophylactic potential of BML-111 in ALI. The gene discussed is FPR2; the disease is acute respiratory distress syndrome.