Because stress granules and STAU1 are degraded by macroautophagy, enhanced translation of mTOR mRNA by STAU1 leads to a maladaptive feed-forward mechanism resulting in greatly reduced autophagic flux.57 Reducing STAU1 by siRNA or genetic interaction can improve autophagy in several neurodegenerative in vitro and in vivo models.58,59 We are currently screening ASOs that target human and mouse STAU1 in models of ataxia and ALS.60 This evidence concerns the gene MTOR and cerebellar ataxia.