Including APOE variants, the contribution of the pathways to the total polygenic risk of AD was 29.6% for β-amyloid metabolism, 26.6% for immune response, 21.6% for endocytosis, 19.5% for cholesterol/lipid dysfunction, 0.3% for angiogenesis, and 2.3% for the unmapped variants (Fig. 4a). The gene discussed is APOE; the disease is Alzheimer disease.