Finally, we found no evidence that schizophrenia or depression causally influence levels of any included immunological proteins/traits, and only weak evidence for a protective effect of bipolar disorder on CRP, IL-13 and IL-17 levels that did not meet the conventional or Bonferroni-corrected evidential thresholds, suggesting that reverse causality is an unlikely explanation for increased inflammation observed in patients with these disorders. The gene discussed is IL17A; the disease is depressive disorder.