The potential pathway of the relationship between NAFLD risk and sUA was related to inflammation, NADPH oxidase subunit-4 (NOX4) associated lipogenesis, production of reactive oxygen species (ROS), NOD-like receptor family pyrin domain containing 3 (NLRP3)-related inflammasome activation, and a cascade of endoplasmic reticulum stress via sterol regulatory element-binding protein 1 (SREBP-1) (11). Here, SREBF1 is linked to metabolic dysfunction-associated steatotic liver disease.