A widely accepted mechanistic hypothesis for AF postulates that the large increase in intracellular oxidative stress observed upon treatment is the consequence of strong inhibition of the selenoenzyme thioredoxin reductase (TrxR); in turn, such severe oxidative stress causes a profound mitochondrial dysfunction ultimately leading to apoptosis.6–8 Yet, some additional targets including NFKB2 and CHORDC1 were disclosed for AF by recent proteomic studies suggesting that AF may possess a more complex, multitarget mechanism.9 The gene discussed is CHORDC1; the disease is atrial fibrillation.