The studies of Gidalevitz et al [16] demonstrating how polyQ deposition alters the folding and function of other proteins provides the first clear experimental support for the hypothesis that aggregation-induced chaperone depletion (e.g., as suggested to explain the toxicity of ALS-mutant SOD1, [65]) can cause cellular dysfunction. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.