A recent study explored a novel role of mTOR complex 1 (mTORC1) in TLR2and TLR4-induced PMN activation (80) . Administration of rapamycin, an inhibitor of mTORC1, decreased the severity of lung injury after intratracheal LPS or PAM (a TLR2 ligand) administration, as determined by diminished neutrophil accumulation in the lungs, reduced interstitial pulmonary edema, and diminished levels of TNF-α and IL-6 in bronchoalveolar lavage fluid. These results indicate that mTORC1 activation is essential in TLR2-and TLR4-induced PMN activation, as well as in the development and severity of ALI.