This interpretation is also in good agreement with the latest two-stage genome-wide association study on 111,326 clinically diagnosed AD cases and 677,663 HC, where pathway enrichment analyses confirmed and expanded on a causal involvement of amyloid precursor protein (APP), tau, and tau-binding proteins in AD pathogenesis, at the same time highlighting the key role of microglial activation and the likely involvement of microglial endocytosis, a mechanism that is also heavily involved in APP metabolism [96]. The gene discussed is APP; the disease is Alzheimer disease.