JM17 has recently been shown to increase expression of proteasome subunits, antioxidant enzymes, and molecular chaperones via actin or the Nrf1/Nrf2 pathway to mitigate toxicity of the mutant androgen receptor responsible for SBMA in cell, fly, and mouse models [26]; however, the detailed mechanism of action in neurodegenerative diseases such as SCA3 remains unknown. This evidence concerns the gene ATXN3 and neurodegenerative disease.