We have previously reported that iNOS plays an important role in multiple features of septic ALI in the murine CLP-sepsis model, including pulmonary microvascular endothelial barrier dysfunction and the resulting albumin hyper-permeability, pulmonary oxidant stress, pulmonary microvascular PMN sequestration and trans-PMVEC PMN migration [17, 18, 35, 47]. The gene discussed is NOS2; the disease is Sepsis.