Our previous work in human atrial myocytes from patients with AF showed that preventing binding of miR-31 to dystrophin mRNA not only restored dystrophin protein content but partially recovered NOS1, in the absence of changes in NOS1 mRNA,7 indicating that dystrophin affects NOS1 protein stability as well as its subcellular localization. The gene discussed is NOS1; the disease is atrial fibrillation.