The pathogenesis of liver dysfunction has not been defined, but we propose that it may be related to the following factors (18): (1) direct damage from excessive TH, (2) inhibited activity of glucuronyl transferase (UGT) in the liver, (3) disturbed excretion of serum bilirubin, (4) development of cholestatic jaundice, (5) relative lack of oxygen in the liver under a hypermetabolic condition, (6) thyrotoxicosis affecting the activities of various enzymes in the liver, (7) liver damage caused by autoimmune reactions. The gene discussed is SLC35A2; the disease is obstructive jaundice.