Duchenne muscular dystrophy (DMD)—which is caused by mutations in the dystrophin gene—is one of the most severe myopathies. Among therapeutic strategies, exon skipping allows the rescue of dystrophin synthesis through the production of a shorter but functional messenger RNA. Here, we report the identification of a microRNA—miR‐31—that represses dystrophin expression by targeting its 3′ untranslated region. In human DMD myoblasts treated with exon skipping, we demonstrate that miR‐31 inhibition increases dystrophin rescue. These results indicate that interfering with miR‐31 activity can provide an ameliorating strategy for those DMD therapies that are aimed at efficiently recovering dystrophin synthesis.