Importantly, the formation of NETs during sepsis is trigged by microbial components or endogenous danger signals, and regulated by complex mechanisms presumably including HMGB1-TLR9-MyD88 pathway.491,492 NETs activate STING pathway in endothelial cells via TLR2 and cause inflammation and coagulation in the lungs, thereby contributing to the poor outcome of sepsis-induced ALI.493 Exogenous administration of NETs further aggravates lung injury, which could be reversed by STING inhibitors or knockdown of STING.494. This evidence concerns the gene TLR2 and Sepsis.