The DM1 cardiomyopathy therapeutic landscape is mature and broad: ASOs are the furthest along as DYNE-101 and IONIS’s ASOs are in advanced clinical trials and show robust target engagement and splice correction in muscle and heart tissue; CRISPR-based approaches, while conceptually powerful, are still in development due to the technical challenges of precisely excising large CTG repeats of mutant DMPK, achieving efficient and tissue-specific delivery, and mitigating off-target risks. Here, DMPK is linked to myotonic dystrophy type 1.