In contrast, in patients with SLE, a subset of anti-double-stranded DNA antibodies that cross-react with NMDAR, originally described to bind GluN2A and GluN2B subunits in their open configuration [74], have more recently demonstrated preferential increase of synaptic transmission through GluN2A [25]. The gene discussed is GRIN2A; the disease is systemic lupus erythematosus.