Notably, lipid droplet accumulation in MUP-uPA/Atf4Δhep livers was reduced relative to MUP-uPA/Atf4F/F livers (Fig. 5E), a situation typical of advanced human NASH.3,52 ATF4 ablation also accelerated and augmented HCC development, which was not apparent in MUP-uPA/Atf4F/F mice of a similar age (Fig. 5D), and increased lipid peroxidation (Fig. 5E). This evidence concerns the gene ATF4 and metabolic dysfunction-associated steatohepatitis.