This transition towards disease-associated microglia (DAM), which occurs with the progression of the disease, is characterized by a distinct transcriptomic fingerprint, which features the downregulation of homeostatic genes (e.g., purinergic receptors, Cx3cr1 and Tmem119) and the concomitant upregulation of AD-related genes such as ApoE, cathepsin D (Ctps), lipoprotein lipase (LPL), tyro protein tyrosine kinase binding protein (TyroBP) and Trem 2 [40]. The gene discussed is LPL; the disease is Alzheimer disease.