The pathophysiology underlying atrial fibrillation (AF), the most common sustained cardiac arrhythmia, traditionally has been viewed as secondary to external atrial stressors rather than reflecting a primary atrial disorder.1 Prominent risk factors such as hypertension, obstructive sleep apnea, and ventricular cardiomyopathy have generally been assumed to exert hemodynamic strains leading to atrial dilation and arrhythmia vulnerability.2 Although increased atrial filling pressures and associated stretch may be contributors, our evolving understanding of AF pathogenesis has begun to suggest more nuanced underlying pathways that may be mediated by primary genetic disease.