A central regulator of metabolism and autophagy in both invertebrates and vertebrates is TOR (Target of Rapamycin) kinase, and inhibition of TOR kinase activity by rapamycin and its analogs has been used successfully to stimulate autophagic clearance of mutant htt aggregates in both Drosophila and mouse models for HD [48]. The gene discussed is HTT; the disease is Huntington disease.