Patients with symptomatic atrial fibrillation (AF) often undergo catheter ablation, during which pulmonary veins are electrically isolated from the atrium. Many key components of the intrinsic cardiac autonomic nervous system (ICNS) are located in close proximity to ablation sites near the pulmonary veins and might be damaged during the procedure. However, the effect of ICNS injury on treatment outcomes is poorly understood. In a study published in Sci. Transl Med., patients who showed greater release of S100B, a neuronal injury marker produced by cardiac glial cells during catheter ablation of AF, were less likely to experience recurrent AF compared with patients who had minimal increases in this neuronal marker. S100B is released upon damage to the ICNS and can induce neurite outgrowth in intracardiac neurons. These findings show that S100B release from glial cells is an indicator of acute intracardiac neural damage during AF. “Further studies should assess the value of targeting the ICNS during ablation and impact on patient outcomes,” conclude the investigators.