IL23A and systemic lupus erythematosus: While our study of gene expression levels in PBMC from SLE patients did not completely replicate our findings in the GILZ-deficient and GILZ-Lyn double-deficient mice, GILZ was robustly negatively correlated with expression of IL23A, an important Th17 driver, and with BAFF and IL18 when studied in the subset of glucocorticoid-free patients.