Therapeutic approaches for polyQ diseases. Although no effective disease-modifying therapies are currently available, several promising strategies are under development. These approaches target different levels of pathogenesis. At the DNA level, CRISPR/Cas9 and base editing approaches seek to correct the CAG-expanded tract or insert CAA interruptions. ZFP-TFs aim to reduce transcription of the disease gene. As the mutant RNA undergoes aberrant splicing, splicing modulators correct aberrant RNA processing. Additionally, RNA-based therapies such as ASOs and miRNAs target mutant transcripts for degradation or repress translation. At the protein level, conformation stabilizers and aggregation inhibitors help prevent protein misfolding and inclusion formation, while caspase and calpain inhibitors prevent cleavage of the mutant protein into toxic fragments. Finally, autophagy-inducing compounds enhance clearance of misfolded proteins (created in BioRender, https://BioRender.com/4l83pge).