Breach of the BBB, neutrophil activation, transmigration and subsequent intrathecal and peripheral release of NETs are thought to act in concert with neuropathogenic autoantibodies including anti-NR2A/B antibodies to cause inflammation and neuronal cell death, leading to neuropsychiatric manifestations of SLE (191). The gene discussed is GRIN2A; the disease is systemic lupus erythematosus.