Considering that Aim2 gene deficiency in the mice is predicted to increase the expression of T1 IFN-β and activate a T1 IFN response [50, 51] and activation of the T1 IFN response in microglia increased Trem2 mRNA levels [79], which encodes for the TREM2 receptor that regulates microglial functions (including phagocytosis of Aβ deposits) [80], it is conceivable that the Aim2 gene deficiency reduced the Aβ deposits in the Aim2−/−.(B6.Sv129); 5XFAD AD mouse model through upregulation of the Trem2 gene expression. This evidence concerns the gene IFNA1 and Alzheimer disease.