ATP7B and Wilson disease: This substantial heterogeneity likely resulted from variations in species (humans, mice, rats, dogs), WD models (including diagnoses of WD in humans, Atp7btx/tx, Atp7b−/−, Long–Evans Cinnamon, Long Evans Agouti Piebald, and TX–J/TX–R mouse models), ages of subjects, tissue preparation techniques, and the specific mitochondrial measures (such as copper levels, enzyme activity, and morphology).