Age does not spare the liver. We reviewed here the essential actual knowledge about age related modifications of this organ. Liver volume and blood flow decrease with age. Aging is also associated with a decline in the intrinsic metabolic activity of the hepatic parenchyma, and in the gene expression of proteins involved in intermediary metabolism, mitochondrial respiration and drug metabolism. Aged hepatocytes accumulate oxidative DNA damage, responsible for the increase in mutations, particularly in the mitochondrial genome. Histologically, aged hepatocytes are characterized by accumulation of ageing pigments into the cytoplasm and by pseudocapillarization of the sinusoid. Age is also of importance at the time of HCV infection: fibrosis progression is faster when the virus is acquired after 40 years. In liver transplantation, an old transplanted liver is now an identified cause of primary non-function of the graft and an independent cause of mortality after transplantation. The age of the donor is also a predictive factor of the severity of recurrent liver HCV-related disease on the graft.