While there is a mounting body of evidence supporting the role of neuroinflammation in the pathophysiology of ADHD (32) and the role of aberrant complement activity in excessive synapse elimination and the development of schizophrenia (33), our findings of larger amygdala and abnormal behavior in C3aR−/− mice point to the importance of basal complement activity and signaling through C3aR for normal brain development and function. The gene discussed is C3AR1; the disease is schizophrenia.