In supporting this notion, it was demonstrated that in HSF-1-overexpressing worms treated with bec-1 RNAi, a reduction of PolyQ protein aggregation (i.e., a cause of Huntington’s disease) was not observed compared with treatment with empty vector, thereby suggesting that HSF-1 has a role in the autophagic induction that protected the worms against toxicity of the aggregated protein. This evidence concerns the gene HSF1 and juvenile Huntington disease.