Interestingly, experimental hepatic overexpression of TRIM21 during early stages of NASH development (~20 weeks in a NASH diet) was able to ameliorate liver steatosis, suggesting that endogenous TRIM21 levels are not saturated and that pharmacological activation of TRIM21 might be an approach to control hepatic lipid accumulation. The gene discussed is TRIM21; the disease is metabolic dysfunction-associated steatohepatitis.