We have read with great interest the article of Johner and colleagues, 1 which for the first time correlates the pattern of the electrical activity of the coronary sinus (CS) with the propensity to induce sustained atrial fibrillation (AF) after pulmonary vein (PV) isolation. We believe that this study is at the crossroad of two paramount topics, which have driven our AF ablation strategy so far: defining the electrical signature and detailing the anatomical framework of AF perpetuation. Over the last three decades, experimental studies have given further insight into the electrophysiological mechanisms maintaining AF. The functional shortening of the cellular refractory period has proved to facilitate random and unstable reentries that run through the three dimensions of the atrial myocardium: longitudinal dissociation and endo-epicardial asynchrony are now widely recognized as a key electrical substrate for AF perpetuation. 2,3 The years 2004 and 2005 were pivotal for translation into clinical practice, as two studies proposed to target the signature of this electrical substrate, with the expectation of AF termination that would in return be considered as a proof of concept. 4,5 During the next decade, rapid focal activities, spatiotemporal dispersion, and long-fractionated electrograms have been meticulously analyzed and thoroughly ablated in the right and left atria (LA). However, despite the recent help of new technologies aiming for its standardization, electrogram-based ablation has reported disappointing single procedure outcomes in comparison with the impressive termination rate. The main reason for such discrepancy lies in the resulting lesion set, made of patchy scars which provide abutment areas for recurrent reentries and alter crucial paths for interatrial conduction. In our experience, focusing on the sole electrogram analysis to decipher the secrets of the fibrillatory process has eluded the key role of atrial anatomy. By doing so, we have forgotten the basis of our early success in paroxysmal AF treatment: the ability to make a link between one electrophysiological mechanism and its anatomical support. In 1998, our institution set the pace by observing premature ectopic beats that initiated AF and subsequently identifying PVs as their main anatomical origin. 6 A systematic target was distinguished from a chaotic phenomenon, improving sinus rhythm maintenance and procedural reproducibility.Professor Shah is one of the pioneers involved in this seminal work highlighting the key role of the PVs. More than 20 years after, his group returns to the concept of a link between electrophysiology and anatomy: Johner and colleagues 1 show that a distinct anatomical structure, the CS, exhibits higher activation pattern variability when sustained AF is still inducible after PV isolation. The musculature of the CS and its main tributaries, such as the vein of Marshall (VOM) and the great cardiac vein, is anchored to the LA body, like ivy on a wall. The hypothesis that this arborized musculature plays a role in ...