Among the different features of liver damage, they observed areas of necrosis, foci of hepatocellular degeneration and acute inflammation as well as a loss of hepatic architecture, fibrosis and steatosis in both 5-month-old Ercc1(−/Δ) mice and 24-36-month-old wild-type mice, highlighting not only the parallelism between accelerated aging driven by DNA repair defects and normal aging, but also a series of histopathological and functional aging-related liver changes. This evidence concerns the gene ERCC1 and steatosis.