In animal models, the rhythm disturbances of BMAL1 increase atrial HF events by affecting ion channels and calcium homeostasis, and the deficiency of BMAL1 leads to a decreased ability to inhibit fibrosis and oxidative stress, which causes cardiac fibrosis, stiffness, and enlargement, both of which combine to contribute to the onset and progression of atrial fibrillation (AF) [40]. This evidence concerns the gene BMAL1 and fibrosis.