By contrast, sRAGE levels correlated negatively with joint damage and vascular disease in patients suffering from rheumatoid arthritis, probably by acting as decoy receptor for proinflammatory RAGE ligands like S100 protein family members [160] Indeed, in vitro application of sRAGE to human-salivary gland cell lines before addition of proinflammatory S100A4 led to down-regulation of RAGE expression and inhibition of NF-κB activation [161]. The gene discussed is AGER; the disease is rheumatoid arthritis.