TSE disease, also known as glucocerebroside-deposition disease, is caused by a decrease or deficiency of β-glucocerebrosidase, which prevents glucocerebrosides from being broken down into galactocerebrosides or glucose and N-acyl sphingomyelin, and thus glucocerebrosides are deposited in large quantities in the mononuclear macrophage system, causing massive proliferation of tissue cells. As a result, there are various symptoms such as hepatomegaly, splenomegaly, anemia, skeletal pain, and tamponade. Patients present with varying degrees of anemia or trilineage reduction, and osteoporosis is seen on long bone x-ray with flask-like changes in the long bones. The bone marrow is classified as Gosher’s cells with large cytosomes, abundant cytoplasm, onion skin-like pattern, and nuclei that are deviated to one side. Acid phosphatase staining was positive. The final diagnosis is now confirmed by making an assay of B-glucocerebrosidase activity, which is significantly reduced compared to normal. The disease is autosomal recessive, and symptoms can vary greatly due to the degree of enzyme deficiency, which is generally classified into three types: Type I (chronic, non-neurological, adult type) – -This is the most common type. It can develop in both children and adults, and is more common in preschoolers. It has a slow onset and long course, with no symptoms of neurological involvement. The earlier the onset of disease, the lower the enzyme activity. Usually, the activity of glucocerebrosidase in type I patients is 12% to 45% of normal. Type II (acute, neurological type) – mostly develops within 1 year of age, with symptoms appearing as early as 1 to 4 weeks after birth, and the disease varies with the early onset and can die before 2 years of age. In addition to the signs and symptoms of type I, neurological symptoms are evident. Type II patients have the lowest glucocerebrosidase activity, which is almost difficult to measure. Type III (subacute, neurological) – The onset is slower than type II and can occur in infancy. In addition to visceral involvement, there may be 1 mild or moderate neurological manifestation, most of which appear around 10 years of age. Neurological abnormalities are more pronounced. Current treatment of Gaucher’s disease Symptomatic supportive therapy – including support, nutrition, blood or red blood cell transfusion, analgesia, and antispasmodic. Splenectomy is indicated for patients with giant spleen with hypersplenism, aged 4 to 5 years or older. With the promotion of enzyme replacement therapy (ERT), splenectomy is now rarely applied to relieve symptoms. The prognosis is extremely poor due to the aggressive and rapid progression of type 2 disease and the failure of symptomatic supportive therapy to effectively improve the quality of life. Enzyme replacement therapy – β-glucosylcerebrosidase has been used abroad in recent years to treat this disease with certain efficacy. The general condition of the adult type improves after 1 year of treatment, the liver and spleen are obviously reduced, growth and development are accelerated, hemoglobin is increased, platelets are also slowly rising, and pulmonary function can be improved in those with lung involvement. The bone lesions were as usual, but it was found that there was hypocalcemia at the beginning of treatment without an increase in urinary calcium, so it is presumed that it may take a long time for the bone lesions to improve; gene therapy – the normal gene of β-glucocerebrosidase has been tried to be inserted into own stem cells and transplanted into itself, but further research is needed. Allogeneic stem cell transplantation therapy Allogeneic hematopoietic stem cell transplantation therapy Previously, there was no cure for Gaucher’s disease, only symptomatic supportive treatment, but this does not improve the prognosis of survival, enzyme replacement therapy, to a certain extent, can relieve the patient’s symptoms and reduce patient suffering, but the total treatment cost of more than 100,000 per month, the total annual medical expenditure of nearly millions, limiting the clinical treatment, with more and more domestic and foreign in recent years With the continuous progress of bone marrow transplantation at home and abroad in recent years, the only method that has the potential to improve the prognosis of patients’ survival or even a great possibility of curing Gaucher disease is still allogeneic stem cell transplantation therapy, which brings light and hope to patients. Bone marrow stem cell transplantation therapy can increase enzyme activity, shrink liver and spleen, and reduce Ghoshay cells, significantly reduce patients’ symptoms and improve their quality of life. Domestic and foreign reports show that in recent years, umbilical cord blood hematopoietic stem cell transplantation applied to Gaucher’s disease has achieved better efficacy, and its efficiency and efficacy are even better than that of semi-compatible bone marrow transplantation. Compared with bone marrow stem cells and peripheral blood stem cells, newborn umbilical cord blood stem cells have less allogeneic rejection, lower immunogenicity, and 10-20 times the regenerative capacity and speed than the former. Especially for type 1 patients, the disease progresses slowly, there is no neurological involvement, and the prognosis is better among all subtypes of this disease. Taking all factors into consideration, although there are risks and complications associated with hematopoietic stem cell transplantation, stem cell transplantation is still the most effective and valuable treatment for type 1 patients, and should be performed as early as possible to avoid delaying the disease.