The link between IL-23/IL-17 axis and LN is also supported by the observation that high serum levels of IL-23 and IL-17 at baseline predict an unfavorable histopathological response and British Isles Lupus Assessment Group (BILAG)-non-responders had high IL-23, indicating that a number of LN-patients has a Th-17 phenotype that may influence response to treatment. This evidence concerns the gene IL23A and systemic lupus erythematosus.