Although effective TGF-β signaling pathway-mediated ECM formation in the infarct area is necessary to prevent heart rupture, excessive deposition of the ECM in the myocardium may distort its architecture, facilitate the progression of arrhythmia and cardiac dysfunction, and influence the clinical course and outcome in patients with heart failure [28, 29]. Here, TGFB1 is linked to cardiac arrhythmia.