Mechanistic events are similar in animals or humans exposed to high amounts of exogenous copper [92,99] compared to patients with Wilson disease, except for their genetic ATP7B mutations as the basis for this specific clinical liver injury [2,66] and transcuprein/alpha-2-macroglobulin of the blood following intestinal uptake, regulated by demand through intestinal transporters [151]. This evidence concerns the gene ATP7B and Wilson disease.