Fonseca et al. (2004) demonstrated that C1q deficiency in an AD mouse model partly restores synapse integrity pointing out a role of the complement system in AD. More recently, works from Hong et al. demonstrated that microglial C3/CR3 mediates synapse elimination when challenged with oligomeric Aβ (Hong et al., 2016). The gene discussed is CRIPTO3; the disease is Alzheimer disease.