von Loeffelholz et al. showed that compared to patients with non-nonalcoholic fatty liver disease (non-NAFLD), circulating levels of fetuin-A were increased in patients with NAFLD, and Naito et al. reported that fetuin-A induced endothelial dysfunction and promoted macrophage foam cell formation, leading to the progression of atherosclerosis 42,43. This evidence concerns the gene AHSG and metabolic dysfunction-associated steatotic liver disease.