In disease-related pathways, BAG-1 has its function compromised and this causes BAG-1 accumulation, as in the enriched pathway “HSP70 and HSP40-dependent folding in Huntington’s disease”, which in the SOY1.5 group with higher expression would lead to even more ubiquitin–proteasome activation; however, with HD disease, proteasome functionality is impaired and the impairment of proteasome function leads to changes in neurotransmitter systems [81]. This evidence concerns the gene BAG1 and juvenile Huntington disease.