Several studies have investigated the glycosylation profile of such key proteins in AD patients and discovered an abnormality in the glycan profile of AD patients: the highly expressed special N-glycans, bisecting GlcNAc, were found to be more abundant in AD patients with additional reports revealing that such an increase delays β-site amyloid precursor protein-cleaving enzyme-1 (BACE1) degradation (Hwang et al., 2010) and hence promotes AD pathogenesis (Kizuka et al., 2017). The gene discussed is BACE1; the disease is Alzheimer disease.