Both human Alzheimer's disease (AD) and in vitro and in vivo models of AD show increased IFN‐I expression (Mesquita et al., 2015; Taylor et al., 2014), and in vivo studies showed decreased pathology and altered microglial phenotype in IFNAR1−/− × APPSWE/PS1ΔE9 mice (Minter et al., 2016). This evidence concerns the gene IFNAR1 and Alzheimer disease.