Moreover, treating septic mouse with IFN-β can enhance the production of 15-epi-LXA4 and RvD1 in the lungs, thus accelerating the resolution of pulmonary inflammation as mentioned above [139], suggesting that the lipid-mediated ALX/FPR2-centered proresolving pathway initiated by IFNβ has great potential in the treatment of ALI. The gene discussed is FPR2; the disease is acute respiratory distress syndrome.