Human genome-wide association studies (GWAS) have indicated that mutations in HADHA and HADHB are associated with familial hypertrophic cardiomyopathy [51], and mutations in CPT1, ACADM, and ACAA2 genes are associated with impaired mitochondrial fatty acid β-oxidation [52]. This evidence concerns the gene HADHB and familial hypertrophic cardiomyopathy.