However, when we examined phagocytosis in a genotype-specific manner, we found that aggregated Aβ1-42 treatment resulted in impaired phagocytosis only in monocytes from individuals that were homozygous for either the CD33 or SPI1 AD risk variants, revealing a functional impairment dependent on the interaction between genetics and environment (Figure 1b,c, Supplementary Figure S2a). Here, SPI1 is linked to Alzheimer disease.