Fifth, genome-wide association studies (GWAS) have identified multiple phenotypic regulatory loci, such as SLC6A6 variants associated with DCM, which disrupt myocardial energy metabolism, and SMARCB1 variants that destabilize chromatin structure, collectively shaping phenotypic diversity [25–26]; SVIL loss-of-function variants associated with HCM are closely related to reduced energy utilization efficiency in sarcomeres [23]. This evidence concerns the gene SVIL and familial dilated cardiomyopathy.