Therefore, the theory of ‘reduced neurogenic and elevated gliogenic competences' could be a hallmark of schizophrenia pathology.48 With respect to a potential mechanism of elevated GFAP expression in the postmortem brains, several studies have reported that oxidative stress and inflammatory cytokines contribute to the pathophysiology of schizophrenia.49 However, in our postmortem brains, the examined inflammatory markers, IL1B and IL6, were not upregulated in the disease group nor did their expression levels correlate with GFAP levels. This evidence concerns the gene IL1B and schizophrenia.