Arrhythmogenic right ventricular cardiomyopathy (ARVC), also known as arrhythmogenic right ventricular dysplasia, now denoted as ARVD/C, is characterized by the replacement of the right ventricular myocardium with progressive fibrofatty tissue, and often manifests clinically as right ventricular enlargement (manifested as symptoms of cardiac insufficiency), arrhythmias (often with ventricular tachycardia, ventricular fibrillation, etc.) and sudden death. Simply put, this is a genetic disease caused by an autosomal mutation in which the originally normal heart muscle tissue is destroyed and atrophied away and replaced by a structure like fatty, connective tissue, much like a hole in the wall of a home that has been temporarily plugged with a wooden board. This type of disease is being diagnosed more and more with the popularity of cardiac ultrasound and CT and MRI, and is getting more and more attention. After all, the wall plugged with wooden boards is not as strong as concrete, and there is a possibility of short-circuiting and leakage. The normal muscle used to contract is replaced, the heart function will be affected, the direct manifestation is the enlargement of the right ventricle, and even protrude in some weak places, forming ventricular wall tumor, leading to right heart insufficiency, etc.. The normal heart muscle is mixed with these fatty and connective tissues, as if the copper wire is disconnected and short-circuited, and fatal arrhythmias such as ventricular tachycardia and ventricular fibrillation can occur. A similar disease is Duchenne muscular dystrophy, an X-chromosome mutation that causes atrophy of skeletal muscle throughout the body, which is replaced by fatty, connective tissue. A case was reported of a patient, a skier, who suffered from this skeletal muscle dystrophy and also from ARVC. After discovering that he had this disease, this athlete, through diligent research, discovered that he had a mutation in his gene for laminin that could cause both diseases. This type of congenital disease with muscle lesions is still difficult to treat. The patient with ARVC mentioned earlier had undergone radiofrequency ablation several times in top hospitals in China, but still had recurrent episodes of ventricular tachycardia. I am afraid that the greatest difficulty in the treatment of this type of disease lies in: 1. its progressive nature: this feature is somewhat like cancer, which initially infiltrates only a small area and eventually may develop to the entire right ventricular posterior wall, lateral wall and left ventricular posterior wall, which sounds somewhat like the spread of a tumor, but it does not have the most characteristic feature of a tumor, namely anisotropy, and is confined to specific tissues. A successful radiofrequency ablation of one arrhythmia may result in the growth of a new lesion if the disease progresses again. In addition, it has been reported in recent years that the left ventricular myocardium is also involved in more than 50% of patients. The analysis may be due to the fact that the left ventricular myocardium is thicker and its functional impact is not as obvious as that of the right ventricle where the myocardium is relatively thin, so the clinical presentation is usually right-sided. However, there are many patients who present with ventricular tachycardia of left ventricular origin, which is confirmed by MRI/CT to be associated with a left ventricular lesion, even in the absence of right ventricular involvement. The current edition of Braunwald Cardiology has renamed arrhythmogenic right ventricular cardiomyopathy (ARVC) as arrhythmogenic cardiomyopathy (ACM). 2. Its polygenic complexity: more than ten mutation sites have been identified in ARVC, while in Duchenne muscular dystrophy there are more than 70! There was a gene target therapy for Duchenne muscular dystrophy, but it was also difficult to implement because there were too few effective people. With so many complex genetic mutations, many patients may also carry 2 or even more genetic mutations at the same time, and targeted therapy is actually quite challenging. For other treatments, I am afraid that the response to ARVC is presumed to be inconsistent across different types of genetic mutations. But fortunately, what we do know is that this is a genetic disease and only patients carrying the gene mutation are likely to be affected. If patients and their relatives have unexplained black haze, syncope, or even sudden death, or if the diagnosis of ARVC is clear, they should be alert and need to be monitored with cardiac ultrasound, holter, etc. and perfected with cardiac enhancement CT or delayed enhancement MRI. At present, the main treatment is still ICD implantation to prevent sudden death and symptomatic treatment of cardiac insufficiency; catheter radiofrequency ablation can reduce the onset of ventricular tachycardia and also reduce the frequent discharge of the ICD and alleviate the patient’s pain.