The lack of decreased expression of ATP7A in WD fibroblasts after BCS treatment might be a result of the absence of functional ATP7B protein in these cells, thereby reducing the demand for a downregulation of ATP7A. Furthermore, in both types of experiments we found that cultures grown in basic, control medium also led to an increased expression of ATP7A and increased the growth of cells with the wild-type ATP7A. An increase in the ATP7B transcript level after long-term culturing was only observed for the WD fibroblasts. This evidence concerns the gene ATP7A and Wilson disease.