Due to the dualistic role of ATP7B in both the synthesis of the copper-containing protein ceruloplasmin and biliary excretion of copper, defects in its function lead to copper accumulation in the liver and other organs that express ATP7B [16,32,40] because both functions of ATP7B are impaired in Wilson disease due to ATP7B gene mutation [25,26,31,33,41]. This evidence concerns the gene ATP7B and Wilson disease.