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. The gene discussed is TNFSF13B; the disease is systemic lupus erythematosus.