A cohort study including paroxysmal (<7 days) versus persistent (>7 days) atrial fibrillation patients proved that altered expression of TGFβ1, MMP-9, and tissue inhibitor of metalloproteinase-1 (TIMP-1) plays a vital role during fibrosis progression, whereas IL-6 contributes to inflammation events [74]. The gene discussed is TGFB1; the disease is atrial fibrillation.