Mice overexpressing TRIP‐1 in their lung type II alveolar epithelial cells showed normal lung development, increased phospho‐AKT and E‐cadherin, and were resistant to HALI, as evidenced by less TGFβ activation, apoptosis, alveolar macrophage influx, and KC expression, suggesting a TRIP‐1‐mediated molecular pathway affording protection against acute epithelial lung injury. The gene discussed is AKT1; the disease is medical procedure.