In contrast, neither rhTRX or ORP100S were able to rescue LS1034 p53‐mutant cells, consistent with the inability of mutant p53 to transactivate MDM2 and p21 expression.[75] While differential crosstalk between endogenous TRX and wildtype or mutant p53 might occur due to redox function, because C35S mutant TRX lacks intracellular redox cycling it is unlikely that ORP100S would exert differential protective effects in mutant versus wildtype p53 cancers. Here, TXN is linked to cancer.