Administration of 15d‐PGJ2 attenuated ConA‐induced ALI by inhibiting autophagy flux and mitochondrial ROS and the release of inflammatory factors (TNF‐α and IL‐1β) while up‐regulating the expression of the antioxidative stress factor HO‐1 in mouse models.57 The gene discussed is IL1B; the disease is acute respiratory distress syndrome.