In a dog model, ventricular tachypacing-induced heart failure enhanced Ca2+/calmodulin-dependent protein kinase-II (CaMKII)-mediated phosphorylation of phospholamban (PLB), which further increased the sarcoplasmic reticulum (SR) Ca2+ load with spontaneous Ca2+ transients and triggered activity in the left atrium (LA). This evidence concerns the gene PLN and heart failure.