The IPSS-R score is the basic tool to guide treatment. In general, lower-risk MDS is treated with low-intensity therapy to improve hematopoiesis, improve quality of life and even prolong survival; MDS in the medium- to high-risk group is treated with high-intensity therapy, including chemotherapy and allogeneic hematopoietic stem cell transplantation (Allo-HSCT), with the main goal of obtaining remission and improving survival. I. Supportive therapy Patients with severe anemia can be transfused with concentrated red blood cells, and platelets should be transfused when PLT is 10×109/L or with bleeding risk factors. Multiple transfusions can lead to iron overload in the body, causing fibrosis and functional damage to the liver, heart, endocrine glands and other organs, and even hemochromatosis (blood chromatosis). The serum ferritin level should be tested regularly and treated with iron chelator when appropriate. (a) Androgens such as testosterone undecanoate and stanozolol may be effective for a small number of lower-risk MDS. (B) Hematopoietic growth factors 1, granulocyte colony-stimulating factor (G-CSF), granulocyte-monocyte colony-stimulating factor (GM-CSF): promote granulocyte maturation and release, assist in anti-infection. 2. Erythropoietin (Epo): used for the treatment of anemia in lower risk groups of MDS, generally taking high-dose Epo, 30,000-60,000 U/week, which can be used in combination with G/GM-CSF. Induction of differentiation and pro-apoptosis therapy Some trials have tried all-trans retinoic acid and 1,25-dihydroxyvitamin D3 to induce differentiation in the treatment of MDS, but the efficacy is not exact. Immunosuppressive and immunomodulatory therapy (a) Immunosuppressive therapy (IST) Cyclosporine (CsA) alone or in combination with anti-human thymocyte immunoglobulin (ATG) for MDS in the lower risk group may be better for those who are younger (60 years old), with reduced myeloproliferation, expressing HLA-DR15 (DR2), with normal cytogenetics, and with small PNH clones. However, some MDS patients have disease progression and AML transformation after IST, and IST for MDS is controversial. (ii) Immunomodulatory therapy (IMiDs) Lenalidomide can inhibit the release of inflammatory factors such as tumor necrosis factor (TNF-α) and angiogenesis, promote the activation of T cells and NK cells, and play an immunomodulatory role, which is effective in transfusion-dependent low-risk MDS, especially in patients with 5q-MDS. However, lenalidomide may promote conversion to AML in the presence of complex karyotypes and P53 mutations. Epigenetic modification therapy 5-aza-2-deoxycytidine (decitabine) can inhibit DNA methyltransferase and release the hypermethylation of oncogenes, thus promoting tumor cell differentiation and apoptosis. It can be used for all FAB subtypes of MDS and for those with an IPSS score of at-risk-1 or higher. Optimization of decitabine dose and regimen is ongoing. Survival after 5-azacytidine treatment was superior to conventional therapy, including supportive therapy, low-dose cytarabine and intensive induction therapy, in different subgroups of MDS patients. Epigenetic modification therapy improves hematopoiesis, delays AML transformation, and improves quality of life and survival time. Combination chemotherapy For MDS above RAEB with good general condition and young age, combination chemotherapy can be considered, commonly used are anthracyclines and cytarabine, etc. The remission rate is no less than epigenetic modification therapy. However, for patients with older age, poor general condition, combined with cardiopulmonary disorders, etc., low-dose chemotherapy, such as CAG and HAG prestimulation regimens, is more likely to be indicated. VII. Allo-HSCT Allo-HSCT is the only possible cure for MDS. Consider Allo-HSCT in the following cases: intermediate-risk-2, high-risk MDS, bone marrow primitive cells <5%> with high-risk cytogenetic abnormalities, severe multilineage cytopenia, severe transfusion dependence (even if IPSS score is low). For those who are young and in good general condition, clear-marrow Allo-HSCT is used; for those who are older and in poor general condition, non-clear-marrow Allo-HSCT with reduced dose intensity is used. [Prognosis] MDS may be stable for a long time, with no or only a mild increase in the percentage of primitive cells in the bone marrow, and the patient survives for several years or more than a decade; or the disease may suddenly progress, with a rapid increase in primitive cells and Some patients with MDS may have a sudden progression of the disease, with a rapid increase in primitive cells and transformation to AML; others may have a gradual increase in the number of primitive cells in the bone marrow, with a slow but irreversible progression of the disease to AML.