For example, inhibiting miR-21—an miRNA associated with enhanced fibrosis in AF—using anti-miR-21 in cultured human atrial fibroblasts exposed to media from tachypaced HL-1 atrial cardiomyocytes significantly reduced markers of activated fibroblasts, including α-smooth muscle actin and connective tissue growth factor [12]. The gene discussed is CCN2; the disease is atrial fibrillation.