Indeed, in the same study, monitoring the level of 1 HO‐1, considered a readout of Nrf2 activation, they observed that oxidative stress induced by TrxR1 inhibition occurred at lower concentration of AF (0.25 μM) compared to HCT116 cells IC50 (1.5 μM) and for this reason it should be considered the dominant mechanism underlying AF cytotoxicity. Here, TXNRD1 is linked to atrial fibrillation.