TGFB1 and atrial fibrillation: A gene therapy approach targeting TGF-β1 signaling in AF significantly reduced fibrosis in a canine model; specifically, plasmid-mediated expression of a dominant-negative TGF-β type II receptor in the posterior left atrium decreased fibrosis by 50%, reduced AF inducibility, lowered conduction heterogeneity, and reduced the maximum slope of the action potential restitution curve (from 3.10 ± 0.78 to 1.09 ± 0.17) compared to controls [55].