Since dietary high fructose is a risk factor for non-alcoholic fatty liver disease [5], which affects the functioning and viability of hepatocytes [7, 53], we measured HFrD-mediated liver injury in eIF2α phosphorylation-deficient (A/AHep) mice indirectly from the levels of serum ALT and AST. This evidence concerns the gene GPT and metabolic dysfunction-associated steatotic liver disease.