Interestingly, studies have shown that the glycosylation pattern in this rare disease-associated TREM2 variant differs from the one seen in wild-type TREM2, having increased terminal glycosylation with complex oligosaccharides in the Golgi and decreased solubility, potentially affecting the function and ligand binding of the receptor, and in this way contribute to AD pathogenesis (Park et al., 2017). The gene discussed is TREM2; the disease is Alzheimer disease.