It is also well-established that the stimulation of its receptor EGFR by Aβ1–42, is one mechanism that promotes AD pathogenesis [96], and pharmacological inhibitors against EGFR have been shown to improve memory behavioral outcomes in Drosophila and murine models [74], as well as reduce Tau-induced neuroinflammatory response, microglia and astrocyte activation, and Tau hyperphosphorylation [97]. The gene discussed is MAPT; the disease is Alzheimer disease.