Increased levels of KP metabolites (kynurenine, 3-hydroxy-kynurenine, 3-hydroxynthranilic acid, and QUIN) in cortex and hippocampus of these murine models suggested that activation of the KP might among the potential pathophysiological mechanisms responsible for neuropsychiatric symptoms of SLE (NP-SLE) (161). The gene discussed is NPPA; the disease is systemic lupus erythematosus.