ATOX1 and Wilson disease: Atox1 interacts with Wilson ATPase in an atox1-dependent fashion, and mutations that conserve copper-binding domains (an amino terminus of Wilson ATPase) lead to decreased atox1 binding; these observations suggest that impaired delivery could be the source of Wilson’s disease in patients carrying such mutations, thus making atox1 an essential copper chaperone that plays critical roles in copper homeostasis regulation and homeostasis regulation [113].