It has been reported that Dex can restrain lung tissue inflammatory response in various pathological settings such as sepsis, hemorrhagic shock, and ischemia-reperfusion [26–28]; our previous studies also confirmed that TNF-α and IL-1β concentrations in lung tissues are significantly increased in LPS-induced ALI models, while Dex reduces TNF-α and IL-1β concentrations [17]. The gene discussed is TNF; the disease is acute respiratory distress syndrome.