Since TRX in the reduced form does not interact directly with wildtype p53 even though TR activity is required for transactivation by human p53 in vitro,[73] TRX‐mediated p53 transactivation control is most likely indirect, as has been shown for Ref‐1.[74] Furthermore, our data demonstrate that rhTRX, but not ORP100S, attenuates the ability of chemotherapeutic agents to cause increased expression of p53 and its downstream transcriptional targets MDM2 and p21 only in p53‐wildtype cancer cells. The gene discussed is MDM2; the disease is cancer.