Thus, it is intriguing to speculate that targeted interventions in large animal models of obesity and supraventricular arrhythmias that prevent either (1) mTOR activation (drugs that promote reduced protein synthesis or decrease cardiac or systemic lipid levels) or (2) pathological increases in IKr channel function (cellular mediators that reduce channel opening) may be antiarrhythmic and, therefore, beneficial to obese patients that display vulnerability to atrial arrhythmogenesis. The gene discussed is MTOR; the disease is obesity disorder.