The loss of glycosylation is known to occur in many disease states (Ohtsubo and Marth, 2006) and our observed loss of glycosylation of VMAT2 (a marker of monoaminergic neurons) concurrent with a relative increase in the glycosylated 5-HT2C receptor (i.e., active, membrane-associated) support the complexity of glycosylation events observed in AD (Frenkel-Pinter et al., 2017). The gene discussed is SLC18A2; the disease is Alzheimer disease.