Although auranofin’s clinical effects in suppressing the inflammatory component of RA are attributed to its inhibition of redox enzymes like thioredoxin reductase [145], it is intriguing that this compound also activates TRPA1 (at least in vitro), an effect that would theoretically increase pain and joint degradation given the evidence for its role in arthritis pathogenesis. The gene discussed is TRPA1; the disease is rheumatoid arthritis.