Since current theories deem the formation of Aβ senile plaques and Tau neurofibrillary tangles as clinico-pathological features of AD instead of the causes of AD (Armstrong, 2013), the crosstalk between exosomes and AD-related genes including APP, presenilin (PSEN), and apolipoprotein E (ApoE) has been given with more and more emphasis (Perez-Gonzalez et al., 2012; Fernandes et al., 2018; Fyfe, 2019; Peng et al., 2019). The gene discussed is APOE; the disease is Alzheimer disease.