According to our results, increased risk for schizophrenia could plausibly be exerted via the direct effects of the infection of the brain (circuitry distortion via cyst formation and direct inflammatory factors effects, among others) and/or via neurochemical changes such as increased dopamine mediated by both poor COMT activity and increased dopamine synthesis caused by T. gondii infection. The gene discussed is COMT; the disease is schizophrenia.