Although different pathogenic mechanisms may contribute to DM1 disease,1, 11, 12 large experimental evidence converges in assigning the main toxic function to the expanded DMPK transcripts that sequester members of the muscleblind‐like (MBNL) family of RNA‐binding proteins in cell nuclei forming typical nuclear foci in cells of DM1 patients. Here, DMPK is linked to myotonic dystrophy type 1.