Current developments in (i) the synthesis of new chelator molecules that have a higher specificity for Cu as opposed to Zn and (ii) in the induction of MT1X by alternate drugs that are not chelated by DPA [35], [43] may have a great potential to ameliorate the survival of hepatocytes lacking ATP7B and improve overall efficacy of the therapy in patients having WD. Here, MT1X is linked to Wilson disease.