The stepwise increase of senescence (p53, p16), prothrombotic (TF), and proremodeling (MMP-9) markers observed in the right atrial appendages of patients in SR, PAF, and PmAF points toward multiple interactions in the human atrium that enhance the senescence burden, atrial extracellular matrix remodeling, thrombogenicity, and other putative mediators involved in the progression of AF. This evidence concerns the gene TP53 and atrial fibrillation.