A previous study reported that the cortical brain tissue of human patients with Alzheimer’s disease (AD) has considerably decreased OGT levels [1], implying that O-GlcNAcylation modification plays a critical role in the maintenance of neuronal health, and that dysfunction of O-GlcNAcylation likely contributes to the pathophysiology of neurodegenerative disorders [1]. The gene discussed is OGT; the disease is Alzheimer disease.