In Alzheimer’s disease, for example, GWAS-identified risk loci such as APOE, BIN1, and CLU affect chromatin accessibility and transcription factor binding in microglia, ultimately influencing tau aggregation and amyloid-beta clearance.58 However, a standard eQTL-based approach may identify a SNP influencing BIN1 expression but fail to capture downstream proteomic interactions, such as tau phosphorylation, that ultimately drive disease progression. This evidence concerns the gene BIN1 and early-onset autosomal dominant Alzheimer disease.