In more detail, clinical studies on stem cell transplant recipients or individuals with familial DNMT3A mutations have demonstrated several correlations with cardiac abnormalities, suggesting that they are explained mainly by secondary factors (transplant-related stress and inflammation) rather than the mutation itself; therefore, although DNMT3A mutations do not directly cause AF, they affect its pathogenesis through inflammatory pathways and signaling pathways [124,125]. Here, DNMT3A is linked to atrial fibrillation.