As the rate of cognitive decline in preclinical AD is significantly increased by the presence of APOE ε4, with some reports showing that Aβ+ ε4 non-carriers do not show any decline in cognitive function even over 4-5 years, it is imperative that current secondary prevention clinical trials in preclinical AD consider the ε4 status of individuals enrolled. This evidence concerns the gene APOE and Alzheimer disease.