We showed that CD4+CD25+Foxp3+ Tregs resolve experimental ALI by modulating critical prorepair steps: (a) abrogation of macrophage proinflammatory responses, (b) augmentation of neutrophil efferocytosis (29), (c) limitation of fibroproliferation (30), and (d) augmentation of alveolar epithelial repair (31). The gene discussed is FOXP3; the disease is acute respiratory distress syndrome.