Since the transient overexpression of the TrxR1 protein partially reversed this repression, they postulated that TrxR1 may participate in the regulation of PI3K/Akt/mTOR pathway and that high TrxR1 levels can attenuate AF‐induced inhibition of the PI3K/Akt/mTOR pathway. The gene discussed is MTOR; the disease is atrial fibrillation.