Some researchers have put forward the concept of a “telomere-p53-PGC axis”: that is, that the shortening of telomere will activate p53 expression, thereby inhibiting PGC-1 and causing mitochondrial dysfunction and a series of reactions such as oxidative stress and intracellular Ca2+ overload, eventually inducing AF [11, 12, 17, 18]. The gene discussed is TP53; the disease is atrial fibrillation.