As a result RyR2s from spinophilin-1 KO mice showed the expected increase in RyR2 open probability in lipid bilayer experiments, increased Ca2+ spark frequency in isolated atrial myocytes, which could be reverted by CaMKII inhibition, and most importantly increased atrial ectopy and susceptibility to pacing-induced atrial fibrillation in vivo, which could be reverted by crossing in phosphorylation-dead RyR2-Ser2814A mice (Chiang et al., 2014). Here, RYR2 is linked to atrial fibrillation.