Our major findings showed that: (a) schizophrenia patients showed higher activity of the TLR4/NF-κB/IL-1β signaling pathway but dampened monocytic response to LPS stimulation, as compared to healthy controls; and (b) higher TLR4 levels may contribute to cognitive impairment by possibly affecting the white matter rather than gray matter volume or cortical thickness. This evidence concerns the gene TLR4 and schizophrenia.