Its presence in livers of young children with end stage hepatic disease, characterized by SA- βgal activity accompanied by changes in the classical senescence pathway encompassing activation of p53, p21cip1 and p16INK4a, as found in the present study, support the concept that the loss of replicative capacity of the hepatocytes is related to liver damage. The gene discussed is CDKN1A; the disease is liver disorder.