Moreover, inhibitory pharmacological treatment selectively targeting the RyR2 Ca2+ leak or genetic inhibition of mitochondrial ROS production both prevented atrial fibrillation, indicating that RyR2 leakage and mitochondrial ROS generation may indeed constitute a self-enforcing subcellular cycle that can set off arrhythmias (Xie et al., 2015). The gene discussed is RYR2; the disease is atrial fibrillation.