Also, patients harboring familial AD mutations, such as amyloid precursor protein and presenilin (PS)-1/2, show increased Aβ aggregation rates (Hatami et al., 2017), and mutant PS2 transgenic mice displayed microglial abnormalities, increased TREM2 and IL-6 expression in culture, thus promoting inflammation (S. Fung et al., 2020). The gene discussed is TREM2; the disease is Alzheimer disease.