In agreement with the identification of myofibroblast NOX4 contributing to human fibrotic diseases, including idiopathic pulmonary fibrosis (25), robust NOX4 immunoreactivity was found localized to myofibroblasts in DMD patient muscle (Supplemental Figure 1A; supplemental material available online with this article; https://doi.org/10.1172/jci.insight.158316DS1), identified by costaining for αSMA and vimentin (37). Here, ACTA1 is linked to Duchenne muscular dystrophy.