In the context of schizophrenia, notable correlations were identified between cognitive deficits or positive symptoms and biomarkers of IRS activation, including dysfunction of paracellular adherens junctions (e.g., IgA to E-cadherin and β-catenin) and tight junctions (e.g., IgA to occludin and zonulin), bacterial translocation (e.g., elevated IgA/IgM to Gram-negative bacteria), as well as disruption of the blood–brain barrier (e.g., increased IgA to occludin and β-catenin) (23, 24). This evidence concerns the gene IARS1 and schizophrenia.