“…These observations provide a potential explanation for the observed association between rs4647602 polymorphism and AF. This higher transcription may cause a higher tissue caspase-3 levels in the atrium, which subsequently causes increased apoptosis in the human atrial [15,16,[33][34][35], resulting in atrial fibrosis which is considered a fundamental mechanism in the perpetuation of AF [36,37]. However, it is possible that rs4647602 polymorphism might be a functionally neutral marker that is in linkage disequilibrium with a genetic variant of another gene adjacent to CASP3 gene, or with the true causative locus far away from the CASP3 gene, such as one of the variants identified from reported GWAS data [10].…”