The reduction in AD pathology and reversal of memory deficits observed in AD mice following genetic deletion or pharmacological blockade of mGlu5 is paralleled by an increase in autophagy via alterations in Zinc finger and BTB domain-containing protein 16 (ZBTB16)- and Unc-51-like kinase 1 (ULK1)-dependent pathways (Abd-Elrahman et al., 2018). The gene discussed is GRM5; the disease is Alzheimer disease.