In transfected cells bearing aggregating proteins with polyglutamine (polyQ) expansions, such as caused by the Huntington's disease mutation in which the CAG tract in the Htt gene is expanded or by mutant Ataxin 1 in the case of spinocerebellar ataxia 1, blockade of mTORC1 with rapamycin or pan-mTOR catalytic inhibitors results in stimulated autophagy followed by removal of mutant protein aggregates and cytoprotection [298, 299]. This evidence concerns the gene MTOR and Huntington disease.