Recently, the above Gi-βγ-regulated mechanism implicated in mediating PDE4-dependent proasthmatic changes in contractility in β2AR-desensitized ASM was also found to mediate the in vivo airway hyperresponsiveness and inflammation elicited by inhaled antigen challenge in a rabbit model of allergic asthma [18]. The gene discussed is ADRB2; the disease is allergic asthma.