Hemophagocytic syndrome (HPS), also known as hemophagocytic lymphohistiocytosis (HLH), was first reported by Risdall et al. in 1979. Clinical symptoms include fever, hepatosplenomegaly, hematocrit reduction, biochemical changes and histiocytosis. The syndrome is divided into two categories: hereditary and acquired, with the hereditary form mainly due to immunodeficiencies caused by genetic mutations and the acquired form often secondary to infections, tumors and autoimmune diseases. The pathogenesis of HPS in the usual state is mainly due to uncontrolled immune response and ineffective immune response caused by hyperinflammatory state: the body is stimulated by various pathogens, lymphocytes and mononuclear macrophages are overactivated and in a state of uncontrolled, secreting large amounts of inflammatory cytokines, ILC1, IL-6 leading to fever; activated macrophages, TNF leading to liver function damage, hypertriglyceridemia and Activated lymphocytes and histiocytes infiltrate the tissues and organs, leading to the growth of liver and spleen; TNF-α and TNF-r inhibit the proliferation of hematopoietic progenitor cells, resulting in the reduction of hematopoiesis, while the abnormal increase of phagocytes causes the destruction of a large number of blood cells, which eventually leads to the reduction of whole blood cells. The syndrome is dangerous, progresses rapidly, and has a high mortality rate without timely diagnosis and treatment. The clinical diagnosis is based on the diagnostic criteria for hemophagocytic syndrome published by the International Society of Histiocytes in 2004.