Finally, in the context of DM1, where we know the positive contribution of MBLN1 is lost and the inhibitory effects of CUGBP1 are enhanced, the moderate increase in Stau1 levels that we have documented in patient tissues, may not be enough to completely prevent the inhibitory contribution of the Alu elements on exon 11 inclusion (Fig 7). This evidence concerns the gene CELF1 and myotonic dystrophy type 1.