The lack of positive controls such as β3-adrenergic receptor (CL-316,243), PPARα (fenofibrate), and PPARγ (rosiglitazone) agonists with known potential to activate UCP1 and PPARα expression, induce thermogenesis and fatty acid oxidation, and demonstrate anti-obesity effects in rodents is another limitation [57,58,59]. The gene discussed is PPARA; the disease is obesity disorder.