Previous researches indicated that reduced SR Ca2+ load and Ca2+ transient amplitude were responsible for the decreased contractility and relaxation of HF.3 And aberrant density of Ca2+ in cytoplasm can accelerate the remodeling of hearts by induction of atrial fibrillation (AF).4 Impaired release or reuptake ability of ER caused by chronic activation of β-AR through PKA phosphorylation provides a mechanism to explain the therapeutic efficacy of β-blockers in HF.5 Novel therapeutics of HF focused on both RyR2 and SERCA2a are undergoing clinical testing. The gene discussed is RYR2; the disease is atrial fibrillation.