However, the miR-206 control of KSRP expression that we document in the current work promotes an increase in the endogenous expression of utrophin A. This is important, as utrophin A upregulation is currently envisaged as a potential therapy for DMD because it can functionally compensate for the absence of dystrophin along the sarcolemma of dystrophic muscle fibers. This evidence concerns the gene KHSRP and Duchenne muscular dystrophy.