We previously implicated upregulated PDE4 activity due to activation of the βγ subunit of Gi protein in mediating airway constrictor hyperresponsiveness and inflammation in an in vivo rabbit model of allergic asthma [18], as well as the altered contractility elicited in isolated ASM tissues sensitized under various atopic-related and-unrelated proasthmatic conditions [16–18,32]. Here, GNAI1 is linked to allergic asthma.