On the other hand, suppressing the expression of CAV-1/ NF-κB axis can significantly ameliorate ALI by activating autophagy-related AMP-activated protein kinase (AMPK), restraining AKT/mTOR pathway activation, and attenuating inflammatory response in CD4/80+ macrophages and CD3+ T lymphocytes [45], suggesting that CAV-1/ NF-κB axis is a potential therapeutic target for ALI. Here, NFKB1 is linked to acute respiratory distress syndrome.