Despite the strong induction of genes involved in hepatic β-oxidation of fatty acids by TTA, it was evident that the levels of TAG increased in the liver, which is in contrast to the effects reported for most known PPARα agonists in the setting of fatty liver [29–34] However, increased liver TAG levels have earlier been found in rodents fed diets supplemented with PPARα agonists, [35–37],in overweight humans with NAFLD treated with fenofibrate [38] as well as in HFD fed hTNFα transgenic mice supplemented with TTA [39]. This evidence concerns the gene PPARA and metabolic dysfunction-associated steatotic liver disease.