DMPK and myotonic dystrophy type 1: A 2020 study further confirmed that ASOs targeting non-CUG sequences within the 3’ UTR of DMPK (ISIS 486178) similarly reduced RNA foci and DMPK mRNA levels in the heart and skeletal muscle, improved splicing defects, and reversed key DM1 phenotypes, including muscle stiffness and cardiac conduction abnormalities (161).