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The assumption that it interacts with drugs acting on the renin angiotensin system is weaker than it sounds

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As the liver is the main site for metabolism of dietary copper, dysfunctional ATP7B leads to copper overload in hepatocytes, resulting in liver pathology, and excess copper, not bound to ceruloplasmin, is released into the circulation where it can pathologically accumulate in other tissues, including the brain (Członkowska et al., 2018)