After successful Smad7 knockdown in the AF cells, stimulation of IL-1β did not change the expressions of p-Smad2, p-Smad3, and Smad4. Combined with previous data and studies [25, 40, 41], we believed that Smad7 should be involved in the apoptosis of AF cells by interfering with the formation of the Smad2/Smad3/Smad4 complex and regulate the apoptosis through the mitochondrial signaling pathway. Here, SMAD3 is linked to atrial fibrillation.