Also, consistent with the reductions in hepatic n-3 PUFAs observed in the Adipo-KO mice, diminished n-3 PUFAs have been attributed to NAFLD pathogenesis (74, 75), and their supplementation in diet has shown to alleviate NAFLD by suppressing the sterol regulatory element binding protein-1–mediated lipogenesis, inflammation, and oxidative stress (76–80). This evidence concerns the gene SREBF1 and metabolic dysfunction-associated steatotic liver disease.