Genome-wide association studies have identified genetic loci that contribute to the risk of late-onset AD and show that several of these genes are associated with myeloid cell biology and function (e.g., TREM2, ABCA7, PLCG2, ABI3), implicating myeloid cells in AD pathogenesis.4–7 However, unresolved questions remain about the biological processes involved in myeloid cell dysfunction and eventual disease progression and neurodegeneration. This evidence concerns the gene ABI3 and Alzheimer disease.