In a mouse model of allergic airway disease caused by the inhalation of ovalbumin (OVA), the expression levels of HIF-1α and VEGF increased, and the production of inflammatory mediators, such as IL-4, IL-5, and IL-13, significantly increased, airway hyperresponsiveness and pulmonary vascular permeability increased, which confirmed that the inhibition of HIF-1α could reduce antigen-induced airway inflammation and hyperresponsiveness by regulating VEGF-mediated vascular leakage [80]. This evidence concerns the gene HIF1A and inflammatory response.