A recent study in Alzheimer’s disease showed that complement receptor type 3 (CR3), which is a receptor for soluble FcγRIII, contributes to the phagocytosis and clearance of fibrillar Aβ by microglia, and the internalized Aβ is transported to lysosomes in microglia[12,24]. This evidence concerns the gene CRIPTO3 and early-onset autosomal dominant Alzheimer disease.