We found that STAU1 and molecular target of rapamycin (mTOR) are both overabundant in SCA2 and ALS patient fibroblasts and mouse models associated with abnormal autophagy, which can be rescued by RNAi targeting STAU1, ATXN2, or MTOR (13). This evidence concerns the gene ATXN2 and amyotrophic lateral sclerosis.