Critically, microglia become constitutively activated under inflammatory conditions for example in Alzheimer’s disease in response to Aβ, and we have shown that ANXA1 treatment reduces both in vitro and in vivo the levels of Aβ by increasing its enzymatic degradation by neprelysin and to stimulate Aβ phagocytosis by microglia [147].Pharmacological intervention through exogenous ANXA1 treatment restored microglial surveillance to ensure resolution and maintenance of brain homeostasis; implicating the use of ANXA1 in neurodegenerative disorders [146,147]. The gene discussed is ANXA1; the disease is early-onset autosomal dominant Alzheimer disease.