The mechanisms at the origin of these dysregulations in HF are still not completely understood, but they undoubtedly involve a reduction in the protein level of PPARα [131] and its transcriptional co-activator PGC-1α [132], as PPARα plays a pivotal role in regulating the expression of genes encoding actors of mitochondrial β-oxidation and FA transport [133]. The gene discussed is PPARGC1A; the disease is hydrops fetalis.