Complement factors such as C1q and C3d have been suggested to play a role in various brain diseases.44–46 Recently we showed by a microarray that in brain tissue of GAD-TLE patients, mRNA for C3, C4A and C4B but not for C5 are upregulated and confirmed this by staining for C3d.31 In the present study, we stained for C9neo, which is indicative of functional activation of the membrane attack complex (MAC) and involved in complement-mediated lysis of cells, with negative results. This evidence concerns the gene C3 and generalized anxiety disorder.