To further validate the importance of APOE4 as a partnering risk factor for female sex that promotes the emergence of FDAMic during AD pathogenesis, a matching analysis with the list of upregulated DEGs found in FDAMic (Fig. 3A) was performed against a mouse microglia dataset, from which microglia were harvested from either control or 5xFAD mice of both sexes that had their endogenous mouse ApoE alleles replaced by either the humanized APOE3 (i.e., 33) or APOE4 (i.e., 44) orthologs [114]. The gene discussed is APOE; the disease is Alzheimer disease.