Instead, using transgenic mice expressing the pmEpac1 biosensor specifically targeted to caveolin-rich membrane microdomains, we could show that TAC leads to redistribution of PDE2 and PDE3 between different microdomains which led to augmented β1-AR dependent and reduced β2-AR dependent cAMP signals and contractility [16]. The gene discussed is ADRB1; the disease is persistent truncus arteriosus.