Dunigan-Russell et al., found that auranofin, an FDA-approved drug for rheumatoid arthritis, which was used to inhibit thioredoxin reductase-1 (TrxR1), was observed to activate Nrf2 responses to augment gene expression of HO-1, and thus prevent lung injury in acute respiratory distress syndrome (ARDS) (129). The gene discussed is HMOX1; the disease is acute respiratory distress syndrome.