Increased PDE4 activity has been shown to play a decisive role in mediating the airway constrictor hyperresponsiveness evoked by allergen challenge in asthmatic individuals [19,21] and in animal models of allergic asthma [18,22–26], as well as the pro-asthmatic changes in contractility in isolated ASM tissue that accompanies its prolonged β2AR desensitization [16,17] or passive sensitization with atopic asthmatic serum or IL-13 [18]. The gene discussed is IL13; the disease is allergic asthma.