The existence of different ‘barcodes’ for the rescue of specific aggregation diseases suggests that, although loss of protein homeostasis with aging might contribute to disease initiation (e.g. by HSF-1 abrogation, restoring general protein homeostasis or components thereof), boosting HSF-1 activity is usually insufficient for long-term protection in most dominantly inherited proteinopathies. This evidence concerns the gene HSF1 and proteostasis deficiencies.