This implicates autophagy in mDAN protection, and indeed, genetic autophagy induction (BECN1, TFEB, and LAMP2A overexpression) in α-syn (SNCA) overexpression mouse models ameliorates synaptic and dendritic pathology [325, 458, 459], while induction via rapamycin (mTORC1 inhibitor) treatment in induced pluripotent stem cell- (iPSC-) derived neurons promotes clearance of α-syn aggregates and reduces oxidative stress levels in a paraquat-induced Parkinson's mice model [105, 460]. The gene discussed is TFEB; the disease is Parkinsonism.