Il1b, Arg1, and Nos2 were not altered by IFNAR1 deletion in our study, and these changes along with the suppression of Trem2 in IFNAR1−/− are distinct from profiles in other degenerative models: In the APP/PS1 double transgenic model of AD, disease‐associated increases in mRNA for iNOS were reversed in APP/PS1 × IFNAR1−/− mice, whereas increases in IL‐1 and the “anti‐inflammatory” transcripts for Arg1, TREM2 and TGFβ1 were further increased in the IFNAR1‐deficient mice (Minter et al., 2016). This evidence concerns the gene ARG1 and Alzheimer disease.