Indeed, treatment with the TrxR1 and TrxR2 inhibitor Auranofin—clinically approved for the treatment of rheumatoid arthritis—led to a quicker time-dependent loss of fully-reduced TRX in NE as compared to non-NE SCLC cells supporting pre-existing inhibition of the TRX pathway in NE-A SCLC (Fig. 5c; Supplementary Fig. 7h). The gene discussed is TXNRD1; the disease is rheumatoid arthritis.