The accumulation of cis-diamminedichloroplatinum (II) (cisplatin), which is a chemotherapeutic drug used to treat a variety of cancers, is decreased in many cisplatin-resistant cell lines, and an active efflux pump for cisplatin has been predicted  to exist in some of them. We recently identified copper-transporting P-type adenosine triphosphatase (ATP7B), which is a gene product responsible for Wilson’s disease, is one of the cisplatin efflux pumps and conferred cisplatin resistance consequently. The KB-3-1 cells transfected with ATP7B cDNA possessed resistance to not only copper (2-fold), but also platinum compounds such as cisplatin (8.9-fold), carboplatin (18.2-fold) and nedaplatin (3.5-fold).   The accumulation of cisplatin in the transfected cells was lower than mock-transfected cells, and the efflux of cisplatin from transfected cells was enhanced compared with mock-transfected cells.   ATP7B was overexpressed in cisplatin-resistant prostate carcinoma PC-5 cells compared with their parental PC-3 cells and revertant PC-5R cells. It is also speculated that ATP7A, which is a gene product responsible for Menkes disease, is associated with cisplatin resistance.   Furthermore, yeast and murine copper transporter Ctr1 is also identified as a cisplatin uptake transporter to confer cisplatin sensitivity.   Human Ctr1, however, plays a marginal role in cellular pharmacology of cisplatin. In this review we discuss the functional mechanism and relationship of cellular transport between copper and cisplatin.