It causes changes in the electrical, structural, and neurological properties of the heart muscle, and triggers disease-related changes associated with AF, such as fibrosis.[35] Furthermore, AF can itself induce inflammation during atrial remodeling, thereby perpetuating the arrhythmia in a phenomenon often referred to as “AF begets AF.”[36] In a case-control study of 305 patients with AF and 150 control samples, IL-6, IL-8, IL-10, TNF-α, monocyte chemotactic protein -1 were independently associated with AF (all P values < .05).[37]. The gene discussed is CCL2; the disease is cardiac arrhythmia.