We have previously reported that microRNA-31 (miR-31) up-regulation in the atrial myocardium of patients and animal models with atrial fibrillation (AF) leads to translational repression of dystrophin and accelerated decay of NOS1’s mRNA and that the resulting reduction in NOS1-derived NO contributes to the AF-induced atrial electrical remodelling that promotes the maintenance of the arrhythmia.7 In agreement with these findings, NOS1−/− mice show atrial hallmark features of AF-induced electrical remodelling as well as an increased propensity to develop AF in response to atrial burst pacing.7 This evidence concerns the gene NOS1 and cardiac arrhythmia.