HMGB1 and metabolic dysfunction-associated steatotic liver disease: In this model of NASH, we identified a gradual increase in both endogenous (HMGB1, uric acid, ATP) and exogenous (LPS) danger signals along with up-regulation of their respective receptor sensors, supporting that multiple cumulative danger signals from metabolic insult results in the progression of NAFLD to NASH, fibrosis and liver tumors.