Idiopathic unconjugated hyperbilirubinemia (Gilbert's syndrome, GS) is a relatively common congenital hyperbilirubinemia occurring in 3-7% of the world's population. It has been recognized as a benign familial condition in which hyperbilirubinemia occurs in the absence of structural liver disease or hemolysis, and the plasma concentration of conjugated bilirubin is normal. Recently, it was reported that unconjugated bilirubin exhibited neurotoxicity in the developing nervous system. The 'neurodevelopmental hypothesis' of schizophrenia proposes that an as yet unidentified event occurs in utero or during early postnatal life. We have observed that patients suffering from schizophrenia frequently present an increased unconjugated bilirubin plasma concentration when admitted to the hospital. Therefore, we noticed a relation between unconjugated bilirubin and the etiology of and vulnerability to schizophrenia. Our reported findings suggest that there are significant biological and clinical character differences between schizophrenic patients with and without GS. From the viewpoint of the heterogeneity of schizophrenia, there may be a poor outcome for the subtype of schizophrenia with GS.