PPARA and LCAD are also known to be regulated by PPAR-gamma coactivator-1-alpha (PGC1A) [23], while altered mitochondrial function has been associated with excess levels of plasma FFA in HF patients [24], and in rodent models with excess FA levels not only in plasma but also within the cardiomyocyte [25]–[27]. This evidence concerns the gene ACADL and hydrops fetalis.