This last assumption is based on a study published in 2013 which revealed that HspB5 was able to rescue the folding and compartmentalization of two misfolded transmembrane proteins (Frizzled4-Fz4-FEVR mutant responsible for an autosomal dominant form of familial exudative vitreoretinopathy and ATP7B-H1069Q copper transporter mutant associated with a common form of Wilson’s disease) [75]. The gene discussed is FZD4; the disease is Wilson disease.