Different studies have shown that ASOs have the potential to decrease mutant mRNAs aggregates, leading to the release of MBNL1 and the normalization of different defective alternative splicings in DM1 skeletal muscle cells, and in the skeletal muscle-specific murine model of DM1 [68,136,137]. This evidence concerns the gene MBNL1 and myotonic dystrophy type 1.