Hepatocyte studies suggest that HMGB1 serves as a potent suppressor of hepatic lipid synthesis, protecting against nonalcoholic fatty liver disease through two distinct pathways: sustaining fatty acid β-oxidation processes and alleviating endoplasmic reticulum stress responses [34,35]—effects that stand in opposition to our current observations in adipose tissue. This evidence concerns the gene HMGB1 and metabolic dysfunction-associated steatotic liver disease.