In the murine CLP-septic ALI model, pulmonary microvascular/PMVEC barrier dysfunction in vivo and resulting albumin hyper-permeability developed rapidly over 2–4 h after CLP-sepsis, with a similar time course as PMVEC death, as reflected by PI+ staining, and with specific features consistent with PMVEC apoptosis, including surface phosphatidyl serine presence (Annexin V staining), caspase activation (FLIVO staining), and DNA fragmentation (TUNEL labeling). The gene discussed is ANXA5; the disease is acute respiratory distress syndrome.