These observations imply that positive modulators preferentially acting on KCa3.1 channels (e.g., SKA-31) may not strongly affect KCa2.X channels in atrial myocytes at low doses, or alter cardiac rhythmicity in the absence of arrhythmogenic conditions, such as CPVT. This evidence concerns the gene KCNN4 and catecholaminergic polymorphic ventricular tachycardia.