Limitations in detecting stronger APOE4 allelic dose effects or interactions with these URGs could also be related to differences in sample size of APOE4 carriers in the URGs, accuracy to characterize AD cases and controls in EHR datasets, underestimating AD HRs and interactions due to misdiagnosed cases, inclusion of controls who may have preclinical AD, potential biases in cognitive and clinical assessments, biases in detecting impairment in the different ethnoracial groups and actual differences in the percent of impaired with AD versus non‐AD pathology (e.g., cerebrovascular disease). This evidence concerns the gene APOE and Alzheimer disease.