We base our conclusions on four main observations: (1) FN1 coding variants were present in cognitively unaffected APOEε4 homozygous carriers, but not in affected carriers with clinically diagnosed AD (Supplementary Table 1), and the protective effect was independently replicated is a large cohort of APOEε4 homozygous carriers. The gene discussed is FN1; the disease is Alzheimer disease.