GILZ, also known as the tuberous sclerosis complex 22 (TSC22), is arecently described glucocorticoids (GCs)-induced transcriptional regulatory protein.The marked impact of GCs on GILZ is exemplified by studies showing that (a)dexamethasone markedly increases GILZ mRNA in human rheumatoid arthritis synovialfibroblasts [33], (b) in vivo, GCsincrease GILZ expression while blockade of endogenous GCs inhibits its expression inthe mouse spleen [16], and (c) GILZexpression is reduced in humans in response to reduced circulating cortisol[34]. The gene discussed is TSC22D1; the disease is rheumatoid arthritis.