C4A and schizophrenia: Using an in-vitro model of microglia-mediated synaptic pruning established with patient-derived neural cultures and isolated synaptosomes, Sellgren et al.6 obtained results suggesting that schizophrenia-related risk variants in the C4 locus lead to C4A-mediated excessive complement deposition, which may contribute, at least in part, to increased synaptic pruning mediated by activated microglia in schizophrenia.