Taken together, our data support that Trx2 activity is cytoprotective against hyperoxic injury; however, these results obtained from adenocarcinoma cells may not accurately recapitulate molecular physiologies in vivo due to redox and metabolic imbalances in cell culture models [77, 78], and altered expression of Prx3, Trx2, or TrxR2 which will influence electron flux [79]. Here, TXNRD2 is linked to adenocarcinoma.