The resulting impaired ATP7B function impairs Cu excretion and leads to persistent Cu accumulation in the brain, liver, and other tissues.66 In healthy individuals, hepatic Cu content is generally <55 μg/g dry weight; in patients with WD, hepatic Cu can exceed 250 μg/g dry weight.67 Most frequently, WD patients present with hepatic and/or neuropsychiatric symptoms. Here, ATP7B is linked to Wilson disease.