Various mechanisms of gold (I) agents for anti-RA effects include (1) inhibiting cathepsins K and S; (2) repressing of hydrolytic enzymes such as β-glucuronidase and elastase [169], which play a role in the progression of RA (by aurothiomalate and auranofin) [175]; (3) targeting of thioredoxin reductase (TrxR) enzyme, which modulates cellular processes through the reduction of thioredoxin (Trx) [176,177]; (4) inhibition of leukocyte infiltration [177]; (5) changing macrophage activity [178]; and regulation of the adhesion of neutrophils [179]. The gene discussed is TXN; the disease is rheumatoid arthritis.