In AF, there is damage and remodeling of the atrial myocardium, which increases the expression and secretion of Gal3, causing the production of an extracellular matrix through the TGF-b/SMAD signaling pathway that causes fibrosis of the atrial myocardium, perpetuating the mechanisms that maintain AF with the consequent increase in Gal3 levels [2]. This evidence concerns the gene TGFB1 and atrial fibrillation.