Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, poses a formidable challenge to modern-day medicine. AF affects as many as 5 million Americans (1), and responses to therapy are highly variable among patients. Some therapies are fraught with substantial risk of proarrhythmia. As our population ages, the incidence of this rhythm disturbance, which can be associated with markedly increased morbidity and mortality, will continue to increase. Although strides have been made in elucidating underlying mechanisms, key molecular events remain elusive (2).