Both in vitro and in vivo experiments have demonstrated that the effects of T3- and TRβ-specific agonists are due, at least in part, to induction of hepatic FGF21 and possible suppression of FGF21 in white adipose tissue, providing a mechanistic basis for TH activity in NAFLD therapy [98]. The gene discussed is FGF21; the disease is metabolic dysfunction-associated steatotic liver disease.