That specifically GABAergic synapses are tagged by C1q, engulfed and eliminated by microglia independently of anti-MOG antibodies in the cuprizone model, disconnects the process of C1q-mediated elimination of synapses from the classical role of C1q as recognition molecule of T-cell mediated antigen/antibody complexes that typically occurs in autoimmune diseases as part of the inflammatory response. The gene discussed is MOG; the disease is autoimmune disease.