The pathophysiology of DCM includes myocardial fibrosis, cardiomyocyte hypertrophy, apoptosis, and contractile dysfunction, influenced by factors including genetic mutations [e.g., Troponin T2, Cardiac Type, Titin, Lamin A/C(LMNA), Phospholamban (PLN), Tropomyosin 1, Laminin Subunit Alpha 2], myocardial injury, ventricular remodeling, oxidative stress, and mitochondrial dysfunction, which ultimately leads to heart failure (2). This evidence concerns the gene PLN and familial dilated cardiomyopathy.