Studies of ALI have shown that HIF-1α stabilizes and contributes to the optimization of alveolar-epithelial carbohydrate metabolism in vitro or in vivo models of alveolar injury, and that the absence of HIF-1α in the alveolar-epithelium indicates that lung injury is exacerbated during exposure to ARDS [87]. The gene discussed is HIF1A; the disease is acute respiratory distress syndrome.