Recently, we reviewed the many immune-inflammatory and neuro-oxidative biomarkers that may play a role in deficit schizophrenia, including increased serum/plasma levels of TNF-α, TNF receptors (TNFR), IL-1β and the IL-1R antagonist, CCL2, CCL11, IgA responses to XA, PA and 3OHK, damage markers of the paracellular pathways and tight and adherens junctions, markers of blood-brain barrier breakdown, IgA to Gram-negative bacteria including Hafnei alvei and Klebsiella pneumoniae, malondialdehyde, and advanced oxidation protein products [65]. The gene discussed is IL1B; the disease is schizophrenia.