Thus, we reasoned that the impact of EXOC6B polymorphisms on AD was mainly elicited through the peripheral system and that the EXOC6B rs61619102 homozygous genotype (CC) itself (which was associated with a low level of expression in the peripheral system) interacted with circulating CD34+CD133+ EPCs to reduce AD risk (Table 5; Figure 1D and Figure S5C). Here, PROM1 is linked to Alzheimer disease.