miR-31 is up-regulated in the skeletal muscle of mdx mice, and miR-31 inhibition enhances dystrophin mRNA translation in human DMD myoblasts when dystrophin synthesis is rescued through exon skipping.12 In patients with AF, atrial-specific up-regulation of miR-31 also leads to dystrophin mRNA translational repression and, independently, it accelerates the NOS1 mRNA decay.7 We examined whether miR-31 expression was also increased in the myocardium of mdx mice and if NOS1 expression was altered by consequence. The gene discussed is NOS1; the disease is atrial fibrillation.