Considering the advantages of exosomes, which could be modified with target-specific receptor ligands on the surface, to cross the blood–brain barrier and then be uptaken by autologous cells, corynoxine B was carried by the Fe65-engineered HT22 hippocampus neuron cell-derived exosomes and delivered to the APP-overexpressed neuron cells in the brain of AD mice, where corynoxine B blocked the interaction between Fe65 and APP and induced autophagy, thereby ameliorating cognitive decline and pathogenesis in AD mice (Iyaswamy et al., 2023). The gene discussed is APBB1; the disease is Alzheimer disease.