Aplastic anemia (AA) is traditionally thought of as a “seed/worm/soil” abnormal, hematopoietic failure syndrome caused by physical, chemical, or biological factors. The syndrome actually covers all bone marrow failures, such as AA, paroxysmal sleep hemoglobinuria (PNH), myelodysplastic syndrome (MDS), and immune-related pancytopenia (IRP). In recent years, scholars at home and abroad have made significant progress in the understanding of AA compared with the traditional concept: it is defined that “bone marrow failure syndrome” is not equal to AA, and AA is only one of the syndromes; it is clarified that the main pathological mechanism of AA is hematopoietic tissue damage caused by T-cell hyperfunction, and AA is an autoimmune disease; it is confirmed that The role of immunosuppressive therapy on AA was confirmed. ATG/ALG is an immunoglobulin complex obtained by immunizing rabbits, horses and pigs with human thymocytes/lymphocytes. It is a polyclonal anti-lymphocyte serum with multiple effects on immunologically active cells and hematopoietic cells, and is an immunomodulatory agent. The efficiency of ATG/ALG treatment alone is 40%-70%, and 40%-80% of SAA patients can be removed from transfusion. Some patients with SAA do not respond to the first course of ATG treatment and can be repeated. The onset of action is usually 2 to 6 months after the drug is administered, but it can be early or late (up to 36 months for late onset of action). Common side effects include fever, chills, headache, reduced platelet count, increased bleeding tendency, abnormal liver function, and aseptic osteonecrosis. If adverse reactions such as fever, erythema and urticaria occur during application, adrenocorticosteroid treatment should be applied.