Under normal circumstances, PUFAs act as activators of PPARα and inhibitors of SREBP1c, thereby promoting FA oxidation at the expense of lipogenesis, but in livers of obese patients with NAFLD, PUFA depletion correlates with reduced mRNA levels of PPARA and increased SREBP1c, potentially leading to a pro-lipogenic program that exacerbates the intrahepatic lipid accumulation in these patients.39 Here, SREBF1 is linked to metabolic dysfunction-associated steatotic liver disease.