Whether or not similar mechanisms exist in children remains unclear but highly plausible, given that children generally harbour greater numbers of Hh-producing cells and Hh-responsive cells than adults and that these populations have been shown to expand even in response to relatively minor parenchymal injury, which may make them especially vulnerable to insults that stimulate liver damage and may even go some way towards explaining why simple steatosis has a much less benign course in children than in adults and why advanced fibrosis/cirrhosis can occur relatively rapidly [68]. The gene discussed is HFE; the disease is Cirrhosis.