The severe liver pathology of untreated Wilson disease (WD) is associated with massive copper overload caused by mutations in a liver-specific copper-transporting ATPase, ATP7B. While early, presymptomatic detection and chelation with conventional copper-binding molecules enables effective and life-saving treatment, liver transplantation is the sole option currently available for those with advanced disease. In this issue of the
Stephen G. Kaler
The Editorial Board will only consider comments that are deemed relevant and of interest to readers. The Journal will not post data that have not been subjected to peer review; or a comment that is essentially a reiteration of another comment.