Taken together, the NF-κB, JAK-STAT3, andSmad pathways are central to the pathophysiology of EAT, driving both fibrosisand inflammation and potentially altering the heart’s electrophysiologicalcharacteristics and function, thus fostering the development of AF [86, 87].Targeting the activation of these pathways may offer novel therapeutic strategiesfor AF. The gene discussed is STAT3; the disease is atrial fibrillation.