The proinflammatory mediators derived by eosinophil are major contributors to inflammation in asthma, including airway epithelial cell damage and desquamation, airway dysfunction of cholinergic nerve receptors, AHR, mucus hypersecretion, and airway remodeling, characterized by fibrosis and collagen deposition (Kay, 2005; Watt et al., 2005; Kanda et al., 2009; Walsh, 2010). The gene discussed is AHR; the disease is asthma.