An overview of the demographic data and pathological/ clinical assessments of our ALI study subjects is presented in Tables 1 and 2 . These pulmonary patients were initially identified by study personnel from a search of the Mayo Clinic Arizona Pathology Database with the search key words: lung, biopsy, acute lung injury (ALI), diffuse alveolar damage (DAD), organizing pneumonia, and ARDS. Study personnel subsequently reviewed the available pathology reports and clinical medical records to identify the subset of patients who had received a diagnosis of ALI. Thus, to be included in this study a given patient had to have a diagnosis of ALI and have undergone a biopsy during their course of treatment. It is noteworthy, that this process was not discriminatory and all patients with available biopsy material that had received an ALI diagnosis as part of their standard-ofcare were included in this study. The ALI patients included in this study met AECC established clinical criteria [4] for an acute lung injury diagnosis and also displayed characteristic pathological changes linked with this disease. Specifically, assessments of all study patients upon admission with acute respiratory distress revealed the presence of diffuse radiographic abnormalities and hypoxia characterized by an A-a gradient (PaO2/FiO2) less than 300 [4, 32] . Indeed, the PaO2/ FiO2 ratio in a subset of these cases (11 of 20 total cases) was below 150 and thus would meet clinical criteria for ARDS [4, 32] . In addition, the twenty ALI patients in this study included thirteen patients (independent of PaO2/FiO2 levels) that required mechanical ventilation during their hospitalization. Review of patient medical records also revealed the absence of typical risk factors associated with ALI, including myocardial infarction, pulmonary embolism, infection/sepsis (e.g., pneumonia), and acute drug reaction. The pathology evaluations of all study-subjects confirmed the clinical indications of ALI. That is, each patient included in our study displayed three specific histopathologies in the available biopsies [33] : (i) The presence of fibrin in the alveoli; (ii) The demonstration of an organizing pneumonia (i.e., a prominent airway cellular infiltrate); and (iii) Evidence of reactive airway epithelial Type II cell hyperplasia. Among these twenty ALI patients, 45% (i.e., 9/20) displayed classical diffuse alveolar damage (ALI-DAD). Seven of the study group did not survive hospitalization, and of these non-surviving patients >71% (5/7) received an ALI-DAD diagnosis. A variety of co-morbid medical disorders were evident in our ALI patients, including several patients with connective tissue disorders. However, examination of the medical records and care-giver notes failed to identify elements of commonality regarding disease onset or progression. Nonetheless, the unresolved character of disease progression in these subjects was such that nineteen of the twenty patients received corticosteroid therapy during their course of treatment.