Unlike in LGI1 and Caspr2 encephalitis, no major pathologic effect on individual receptor function or cytotoxic or complement‐mediated effects have been found.24, 25, 52 A question therefore remains why IgG complement–activating subclass antibodies from NMDAR encephalitis patients do not seem to induce complement‐mediated pathology. The gene discussed is CNTNAP2; the disease is encephalitis.