In vivo studies in mice have shown that knocking out the Mgat3 gene, which encodes the N‐acetylglucosaminyltransferase III (GnT‐III) enzyme, resulting in a shift in BACE1 localization toward late endosomes/lysosomes, indirectly targeting the BACE1 activity and reducing Aβ load.[52] While research elucidating the role of BACE1 glycosylation in AD has gained momentum, most approaches still target BACE1 indirectly. The gene discussed is BACE1; the disease is Alzheimer disease.