While experimental evidence points to the critical function of complement in Aβ clearance (Wyss-Coray et al., 2002), and C3- and CR3-dependent microglial phagocytosis appears to play a beneficial role in the elimination of foreign pathogens as well as Aβ (Fu et al., 2012), CR3 also limits Aβ clearance from the brain interstitial fluid (Czirr et al., 2017), and is involved in Aβ-induced microglia-mediated loss of synapses in AD (Hong et al., 2016). This evidence concerns the gene C3 and Alzheimer disease.