Alzheimer disease (AD) has been biologically defined by the accumulation of amyloid in combination with the aggregation of cortical tau, eventually resulting in cognitive decline and dementia.1,2 Several risk factors of amyloid accumulation have been identified, including the ε4 allele of the APOE gene.3 Secondary prevention and disease-modifying therapies for AD are currently being developed and evaluated in numerous clinical trials.4 Here, APOE is linked to amyloidosis.