In terms of the SLE itself being the cause of the neuropsychiatric manifestations, many of them are the result of autoantibody activity: antiphospholipid antibodies (thrombosis, headache, chorea, transverse myelitis, seizures), anti-ribosomal p protein antibodies (psychiatric events), anti NMDA receptor subunits, anti-SM and anti-RNP antibodies (diffuse NPSLE), and anti-AQP4 antibodies (demyelinating lesions).[5] Other incriminated autoantibodies involved in the pathogenesis of NPSLE are anti-endothelial cell, anti-MAP2, and anti-suprabasin antibodies.[1]. This evidence concerns the gene MAP2 and Chorea.