To examine the interaction between AD genetic risk variants and environmental stimuli associated with disease pathology in the periphery, we isolated monocytes from individuals genotyped for SPI1 rs1057233 and CD33 rs3865444 AD risk variants (Supplemental Table S1) and exposed them to aggregated Aβ1-42 in vitro for 24 h to provide a disease-associated stressor. This evidence concerns the gene SPI1 and Alzheimer disease.