We have recently demonstrated that the susceptibility to transesophageal rapid atrial pacing-induced AF and the levels of CaMKII-mediated phosphorylation on serine 2814 were decreased in mice lacking Epac1, a new target of cAMP signaling that is activated independently of PKA, and in mice treated with vidarabine, a cardiac AC inhibitor22,34. Here, CAMK2G is linked to atrial fibrillation.