Understanding the mechanism of this proteolytic stimulation would be important for understanding changes to proteostasis during diseases, such as in cancers where PA28γ expression is upregulated or during Huntington’s disease, where the proteasome is inefficient at degrading proteins with poly-glutamine expanded repeats, which are primarily degraded by the T-L site (33). The gene discussed is PSME3; the disease is juvenile Huntington disease.