Both AHCY’s capacity to bind copper, which is comparable with albumin (Masuoka et al., 1993), and its high abundance in the liver, where it comprises 0.5% of total hepatic cytosolic protein (Bethin et al., 1995), indicate that AHCY could contribute significantly to the hepatic copper metabolism and copper-associated human syndromes, such as Wilson disease. This evidence concerns the gene AHCY and Wilson disease.