Hu et al. [12] demonstrated that activation of mTOR in the epithelium promoted lipopolysaccharide (LPS)-induced ALI, likely through downregulation of autophagy and the subsequent activation of NF-κB signaling pathway, indicating that inhibition of mTOR in pulmonary epithelial cells may represent a promising therapeutic strategy for preventing ALI. This evidence concerns the gene NFKB1 and acute respiratory distress syndrome.