Our results are in line with these findings, revealing a conserved dysregulation in critical calcium channels and associated proteins (S100A8, S100A9, SMOC-2) in AF atria, which may support the synergistic role of abnormal Ca2+ signaling and structural remodeling in failing cardiomyocyte adaptation to abnormal calcium influx and overload derived from rapid atrial stimulation, thereby facilitating the arrhythmia onset and perpetuation [99]. The gene discussed is S100A9; the disease is atrial fibrillation.