(1) The expression of classic homeostatic microglial genes like Cystatin C (Cst3) and Hexosaminidase Subunit B (Hexb), (2) the decrease of other homeostatic microglial genes like Purinergic Receptor P2Y (P2ry12/P2ry13), C-X3-C Motif Receptor 1 (Cx3cr1) and Transmembrane Protein 119 (Tmem119), (3) the distinct increase in lipid metabolizing and phagocytic genes like Alipoprotein E (APOE), lipoprotein lipase (Lpl) and other known AD factors like Cathepsin D (Ctsd), and Triggering Receptor Expressed On Myeloid Cells 2 (TREM2; Keren-Shaul et al., 2017). This evidence concerns the gene TMEM119 and Alzheimer disease.