Similarly, mGluR5 knockout and pharmacological blockade results in delayed disease progression and a reduction in huntingtin pathology in preclinical mouse models of Huntington’s disease (HD) which we have linked to increased autophagy via alterations in both Zinc finger and BTB domain-containing protein 16 (ZBTB16)- and Unc-51-like kinase 1 (ULK1)-dependent mechanisms [13, 14]. The gene discussed is GRM5; the disease is Huntington disease.