This may be related to Angiotensin II triggering the activation of the NLRP3 inflammasome through a Ca2+-dependent mechanism, resulting in the secretion of IL-1β, thereby increasing oxidative stress levels in atrial cells, inducing cardiomyocyte hypertrophy and apoptosis, and consequently enhancing AF susceptibility (163). This evidence concerns the gene IL1B and atrial fibrillation.