NFKB1 and atrial fibrillation: In an experimental model of AF, TMAO produced atrial electric instability, increased AF inducibility, and aggravated the acute electrical remodeling by enhancement of the cardiac autonomic activity and remodeling and activation of the pro-inflammatory p65 NF-κB signaling pathway, showing a mechanism that may play an important role in the perpetuation of atrial fibrillation [247].