MT2A and Wilson disease: These data, supported by biochemical parameters and together with the observation that the mRNA expression of the copper-responsive genes Mt-I and Mt-II was only increased in mice fed a copper-enriched diet for three weeks, suggest that the accumulating copper upon Commd1 deletion is stored safely and does not reach a threshold concentration sufficient to induce hepatocellular toxicity as seen in CT-affected Bedlington terriers and mouse models for WD [9], [10], [36].