Due to the dual role of complement in both phagocytosis and inflammation, the increased production of C1q and C3 in AD has been proposed to cause inappropriate tagging of healthy synapses for removal, that is, “synaptic pruning.” This process has not been fully delineated in adult neurodegenerative disease brains, but a strong link has been confirmed between C1q/C3 and synapse loss in AD mice (Hong et al., 2016). The gene discussed is C3; the disease is neurodegenerative disease.