Nonetheless, FGF21 remains an attractive therapeutic target for treatment of NASH, as numerous preclinical studies have suggested that FGF21 alleviates steatohepatitis and fibrosis in NASH diet-fed mice via decrease of hepatic lipotoxicity, increase of β-oxidation, inhibition of fibrogenesis, or activation of an adiponectin-IL17A axis [83,84,85]. The gene discussed is IL17A; the disease is metabolic dysfunction-associated steatohepatitis.