In recent years, a wealth of new information has been published on the incidence, mechanisms, consequences, and treatment of atrial fibrillation (AF) and the effect of the arrhythmia on quality of life and costs of health care. AF is the most common cardiac arrhythmia, and like prostate cancer in men, the probability of developing AF rapidly grows when a person is past 60 years of age. Despite all that information, our current pharmacological and nonpharmacological means to prevent or control the arrhythmia are frequently disappointing. Often, its presence has to be accepted, and measures to control the ventricular rate and to prevent thromboembolic complications have to be applied. New modes of treatment aimed at preventing the arrhythmia are therefore eagerly welcomed and investigated. In this issue of Circulation , Pappone et al1 describe such a new therapeutic approach in a selected group of patients with AF that uses a transcutaneous catheter technique directed at controlling the mechanism of the arrhythmia. What do we know about AF mechanisms, and does that knowledge help us in selecting a curative approach? Many years ago, Moe2 postulated that AF was based on multiple-reentrant wavelets occurring in random order in the atrium. That theory was subsequently confirmed by mapping atrial activation during AF in animal and human hearts. Fibrotic changes in the atria occurring with aging and atrial dilatation secondary to increased stiffness of the ventricular wall or valvular disease, ischemia, and infiltrative diseases will facilitate the development of a substrate for those multiple-reentrant wavelets. Cox et al3 realized that such a mechanism for AF opened new therapeutic possibilities and developed the maze operation. When several linear incisions were made in both atria, the multiple-reentrant wavelets were no longer possible, and AF disappeared. The results of the maze operation were a stimulus …