Currently, the best theory explaining the pathogenesis focuses on RNA transcripts: in fact, in DM1 cells were found multiple nuclear foci of mutant DMPK-RNA, containing pathogenic CUG repeats, which could produce defects in alternative splicing of multiple RNAs, thus providing a basis for the multisystemic features of DM1 [2]. The gene discussed is DMPK; the disease is myotonic dystrophy type 1.