Importantly, there is some redundancy in decysteinylation activity by several players in the Trx/TRP14 and GSH systems, which may explain the rather low level of protein cysteinylation found in TRP14 knockout mice under basal conditions, as well as in acute pancreatitis when considering a compensatory upregulation in the thioredoxin and GSH system. This evidence concerns the gene TXNDC17 and acute pancreatitis.