In recent studies, siRNA-mediated local or systematical silencing of NF-κB significantly protected animals against further increased proinflammatory cytokine (TNF-α, IL-6) release, histological and other lung injury scores in animals subsequently injured with LPS compared with injury and scramble control, indicating that NF-κB could be a potential target for developing RNAi gene therapy for ARDS (Jin L.-Y. This evidence concerns the gene TNF and acute respiratory distress syndrome.