SOAT1 and atrial fibrillation: Strategies aiming to modulate specific molecular pathways, such as TGF-β, NLRP3, AMPK, JAK/STAT, or/and transglutaminase 2 (TG2) have the potential to mitigate the pathological remodeling underlying the development of the arrhythmogenic substrate for atrial arrhythmias including AF [163].