Thus, based on (i) the significant heritability of AD, (ii) the robust involvement of APOE in AD risk, (iii) a growing body of evidence that cholesterol itself modulates AD risk and (iv) the ontological overrepresentation of cholesterol gene variants in AD GWAS results we hypothesize that SNPs associated with peripheral cholesterol via GWAS also contribute to AD risk. The gene discussed is APOE; the disease is Alzheimer disease.