G0S2 and fatty liver disease: Based on these observations, we made the following hypothesis: (1) palmitate suppresses Nur77 and subsequently stimulates the expression of its downstream target PPARγ and G0S2, (2) this increase in G0S2 expression contributes to palmitate-induced fat accumulation in the liver, and (3) Nur77 overexpression suppresses G0S2 expression in the liver, thereby exerting a protective effect against palmitate-induced hepatic steatosis.