In the setting of AF, these agents may offer dual benefit: (1) electrophysiologic stabilization through the amelioration of Ca2+ mishandling and oxidative stress, which disrupts arrhythmogenic calcium leak from the sarcoplasmic reticulum and (2) structural remodeling attenuation by blunting the inflammasome-induced activation of profibrotic pathways (e.g., TGF-β/Smad and galectin-3 signaling) [202,203]. Here, LGALS3 is linked to atrial fibrillation.