LPS reduced the effective refractory period, widened the window of vulnerability of atrial appendage cells, promoted the expression and lateral distribution of connexin 43, and activated NF-κB signaling via a1-adrenergic receptor (α1-AR) in an animal model of atrial fibrillation, indicating that chronic inflammation represented by LPS may play a role in the atrial fibrillation pathogenesis [253]. The gene discussed is NFKB1; the disease is atrial fibrillation.