1, the current means of treatment: myotonic dystrophy is currently a large group of incurable diseases, but is not untreatable. The existing treatment means for myotonic dystrophy can be divided into symptomatic supportive treatment and allopathic treatment in two aspects. Symptomatic supportive treatment: It is mainly supportive treatment and symptomatic treatment of various complications. The symptomatic supportive treatment of different myotonic dystrophies has both commonality and corresponding treatment measures for different complications. Whether the diagnosis is timely, the timing of intervention, whether appropriate rehabilitation exercises can be carried out in different stages of the disease, and the management of important complications can affect the effect of symptomatic supportive treatment. Take DMD as an example, the ideal symptomatic supportive treatment at present is to adopt regular follow-up and a multidisciplinary joint clinic model, with a medical team composed of neurology, rehabilitation physiotherapy, cardiology, respiratory medicine, nutrition and orthopedic surgeons to provide multifaceted and personalized treatment and guidance to patients and their families. For children diagnosed early, hormone therapy at a basal dose (0.75 mg/kg per day of prednisone) is recommended. Prednisone therapy can help improve muscle strength, prolong independent walking time and improve quality of life. The time of initiation of hormone therapy is usually recommended after vaccination is completed and motor function begins to decline. Allopathic treatment: The only allopathic treatment for myotonic dystrophy caused by genetic mutations is gene therapy. Gene therapy includes two strategies: gene replacement and gene modification therapy. Still using DMD as an example, the strategy of gene replacement therapy transfers the Dystrophin gene into the patient through an appropriate vector to translate the protein and express its function, thus compensating for the patient’s genetic defect. The vector can be stem cells, myogenic cells or adeno-associated virus (AAV), among which the efficacy and safety of stem cell and myogenic cell transplantation are not well established and AAV is the most promising and highly regarded DNA vector. Gene replacement therapy has no requirement for specific mutation types and can be used for patients with DMD with different mutation types. A representative approach to gene modification therapy is exon skipping, which uses antisense oligonucleotides designed to target specific mutation sites so that the translation process skips the mutation site and retains the reading frame, producing a protein that is shorter than normal Dystrophin but retains most of its function, resulting in a conversion from a DMD phenotype to a milder BMD phenotype. Currently, early clinical trials of exon skipping therapy for multiple specific mutation sites have been completed overseas. 2, the current treatment challenges and countermeasures: For domestic patients with myotonic dystrophy, failure to diagnose in time is a common cause of treatment delay and treatment error, and is the biggest obstacle for patients to get effective treatment. Due to the low knowledge of myotonic dystrophy, many patients are misdiagnosed for a long time before the diagnosis, some are misled by some media advertising, the diagnosis is not clear to accept the so-called “biological immunotherapy”, “stem cell therapy”, “nano-technology treatment” and so on. “This wastes a lot of human and material resources, increases the economic burden of families, and causes psychological damage to the children. Solving this problem requires the joint efforts of doctors, basic researchers, patients and families and the whole society. There are still many types of myotonic dystrophy for which the causative gene has not yet been identified, and for these types of patients, the road to effective gene therapy is even longer. There are also many issues that remain to be addressed in gene therapy. Take DMD as an example, the causative gene of DMD, Dyistrophin, is the largest gene in the body, containing 79 exons, and the existing AAV cannot introduce the full-length Dyistrophin cDNA into the body, but only the shortened, partially functional Dyistrophin gene; AAV treatment has the problem of immune rejection, and the application of immunosuppressive drugs Therefore, there is a need to screen for less immunogenic AAV and to find anti-rejection drugs with fewer side effects, and much work needs to be done in this area. The safety of exon skipping therapy is higher than AAV, but it is too targeted. Different deletion mutations require different drugs, and each drug needs to go through a lot of preliminary work such as R&D production, animal testing, and clinical trials before it can really be used for patient treatment, and only a small number of mutations at mutated loci can realize exon skipping therapy at present. CRISPR/Cas technology allows targeted editing of genes by targeted cutting, insertion and modification of specific DNA sequences, which may become the ultimate solution for genetic diseases. The solution. CRISPR/Cas treatment for DMD has shown definite efficacy in animal models, with improved muscle strength, normalization of muscle enzymes, and expression of dystrophin seen in histopathology in treated model mice. However, there are potential risks associated with the treatment, with the possibility of off-target mutations and even recombination at the broken end of the gene, as well as ethical issues associated with gene editing of germ cells, and there are many hurdles to overcome before this technology can be used in the clinic.