Experiments performed in the context of Menkes and Wilson diseases, in which mutations in ATP7A and ATP7B lead to copper deficiency and copper toxicity disorders, respectively, showed that clusterin participates in the degradation of ATP7A and ATP7B (Materia et al., 2011) via the lysosomal pathway (Materia et al., 2012), an observation that tallies with the reported function of intracellular clusterin in facilitating autophagy (Zhang F. et al., 2014). Here, ATP7A is linked to Wilson disease.