Whether GILZ acts as an endogenous inhibitor of inflammation, as suggested by exacerbated imiquimod-induced psoriatic-like lesions in GILZ knock-out mice (63) and increased inflammation upon GILZ knock-down in synovial tissues in a murine model of RA (58), or whether it primarily mediates exogenous GCs effects (43) remains debated. This evidence concerns the gene TSC22D3 and rheumatoid arthritis.