The greater abundance of ACTA1-CUGexp transcripts that we observed in Clcn1 ASO-treated muscles could be interpreted as cause for concern in the translation of this therapeutic approach to DM1 patients, perhaps by increasing the production and/or enhancing the stability of DMPK-CUGexp RNA in skeletal muscle. This evidence concerns the gene DMPK and myotonic dystrophy type 1.