TLR4 and acute respiratory distress syndrome: Qu et al. (68) indicated that HMGB1 binds to certain receptors, such as receptor for advanced glycation end products (RAGE) and TLR4, activates the ROS and phosphatidylinositol-3 kinase (PI3K) pathways and myeloid differentiating factor 88 (MyD88), and results in the release of TNF-α, IL-1β, IL-6, and other cytokines contributing to ALI, suggesting that blocking HMGB1 may provide an effective treatment strategy for AP-associated ALI.