Similarly, our study results provide evidence that NC009-1, NC009-2, and LM-031 are able to interact with both mutant ATXN3 and LC3 to enhance the degradation of mutant ATXN3 by autophagy, and support the concept of applying an ATTEC to treat polyQ-mediated diseases or other neurodegenerative diseases caused by impaired protein quality control. Here, MAP1LC3A is linked to neurodegenerative disease.