Given the fact that protein misfolding and aggregation is common to proteinopathies and modifiers of one proteinopathy can influence another, e.g., a significant fraction of SCA3 modifiers in Drosophila had similar effects in Alzheimer models, we hypothesized that there may exist a subset of genetic modifiers that has broader relevance and may modify several or even all proteinopathies. This evidence concerns the gene ATXN3 and proteostasis deficiencies.