Since then, the idea of liver cirrhosis as a condition of IGF-I deficiency during adult age has been yearly consolidated from a number of publications establishing the origin of this lack from a decrease in GH receptors seen in cirrhotic livers[216] and a progressive reduction of liver synthesis capability from decreased hepatocellular mass in advanced stages[209]. The gene discussed is IGF1; the disease is hyperinsulinemic hypoglycemia, familial, 4.