Since CRP is found to be positively correlated with the onset of AF, and CRP can activate NF-κB pathway through the mediation of TLR4 to induce the secretion of pro-inflammatory factors, NF-κB may also facilitate the enhanced and prolonged activation of TGF-β/Smad signaling in AF. The gene discussed is TGFB1; the disease is atrial fibrillation.