Several potential targets for DM1 therapy have been suggested, including the editing of expanded CTG repeats within the mutant DMPK gene [4,5,6,7,8], degradation of the mutant DMPK mRNA [9,10,11,12] and the correction of RNA-binding proteins involved in DM1, such as MBNL1 and CUGBP1/CELF1 [13,14,15]. This evidence concerns the gene CELF1 and myotonic dystrophy type 1.