A recent 18F-flortaucipir PET study demonstrated that ApoE ε4 had an Aβ-independent effect on the increase in the tau load in the entorhinal cortex and hippocampus [16], while the other studies found this effect was associated with the global Aβ burden [17] or even greater tau burden in the prodromal AD and AD dementia patients without the ε4 allele, particularly in the parietal cortex, than in patients who carried the ε4 allele [18]. The gene discussed is APOE; the disease is Alzheimer disease.