The rate of mitochondrial FA oxidation was lower in the heart in SCD1−/− mice compared with WT controls, which was mainly attributable to a decrease in activity of PPARα and its regulatory pathways [19,20] Interestingly, SCD1 deficiency increased protein levels of PPARα and its coactivator PGC1α in hypothyroidism. The gene discussed is PPARA; the disease is hypothyroidism.