Collectively, the evidence presented suggests that enhancing FOXM1 levels is an effective means to promote cellular proliferation and repair after lung injury and reveals that activation of the p110γ-FOXM1-β-catenin axis in endothelial cells may represent a novel therapeutic strategy for restoring vascular homeostasis, reducing lung edema and treating inflammatory vascular diseases, such as ALI/ARDS; however, further clinical trials are needed. The gene discussed is FOXM1; the disease is acute respiratory distress syndrome.