As bisecting GlcNAc on BACE1 is upregulated in AD patients, and could potentially also be linked to the oxidative stress observed in AD (Kizuka et al., 2016), inhibiting the GnT-III might be an interesting approach to reduce the Aβ load, indirectly targeting the BACE1 activity, yet circumventing the issues of adverse effects seen with BACE1 inhibitors (Kizuka et al., 2017). The gene discussed is BACE1; the disease is Alzheimer disease.