Recanalization is a serious hematologic disorder that mainly manifests as low bone marrow hematopoietic function and reduced whole blood cells. The main symptoms manifest as anemia, bleeding, and infection. The most typical symptom of aplastic anemia is low bone marrow hematopoietic function or even hematopoietic failure, but bone marrow hematopoietic failure is not only one kind of disease, there is one kind of disease called congenital bone marrow hematopoietic failure, which is also a kind of bone marrow hematopoietic failure, let’s learn more about this kind of disease. The clinical manifestations of these diseases may be similar to those of reblastosis and need to be differentiated, but with careful history taking, physical examination and appropriate laboratory tests it is not difficult to differentiate. In children and young adults, the prognosis is not only different, but also the treatment strategy and approach to congenital hematopoietic failure, which is sometimes exceptionally difficult to distinguish. Congenital myelopoietic failure is a rare group of genetically heterogeneous disorders characterized by congenital somatic anomalies, myelopoietic failure and susceptibility to tumors, manifested by peripheral blood allogeneic cytopenia and hypoproliferative bone marrow hematopoietic cells, mainly in Fanconi anemia (FA) and congenital dyskeratosis (DC). . Patients with somatic abnormalities are less likely to be missed, but approximately 20% of FA patients may have no somatic abnormalities, and some patients may not start to develop hematologic changes in their reperfusion until adulthood (the maximum age of onset has been reported to be 49 years), making them vulnerable to underdiagnosis and misdiagnosis. The upper age limit for screening has been revised upwards from 35 years to 50 years. Cells from patients with FA show spontaneous chromosome breaks and are highly sensitive to DNA cross-linking agents such as diepoxybutane (DEB) and mitomycin (MMC). Peripheral blood lymphocytes from FA patients treated with DEB and MMC have significantly more chromosome breaks and are the current gold standard for the diagnosis of FA. Chromosome breakage test can be used for peripheral blood or bone marrow cells, amniocytes, chorionic villous cells, fetal blood cells and skin fibroblasts. In addition, lymphocytes in FA patients are blocked in the G2/M phase and the G2 phase is significantly prolonged. The application of flow cytometry to detect the cell cycle suggests their accumulation in the G2/M phase, which can be used for the diagnosis of FA. Application of immunoblotting assay, any protein deletion in the FANCD2-L core complex will not detect FANCD2-L, enabling rapid examination of protein deletion in the core complex for diagnosis of FA and preliminary determination of possible FA types. The comet test is a single-cell gel electrophoresis for rapid detection of DNA damage and can also be used for FA patients and carriers. In patients with normal lymphocyte DEB test or MMC test and high clinical suspicion of FA, further fibroblast DEB test or MMC test should be performed to exclude false negative lymphocyte DEB test due to FA cell mutations that cause somatic cells to revert to normal. Typical DC patients often show a triad of signs: toenail dyskeratosis, skin hyperpigmentation, and oral mucosal leukoplakia, which is easier to diagnose; patients who show bone marrow failure without obvious physical abnormalities are more difficult to diagnose. The telomere length of each subpopulation of leukocytes in peripheral blood by flow cytometry and fluorescence in situ hybridization is currently the best diagnostic method, and the combined telomere length analysis of each subpopulation of leukocytes (total lymphocytes, CD45RA+/CD20-naive T cells, and CD20+ B cells) is highly sensitive and specific for the diagnosis of DC, and can be used to differentiate it from other bone marrow hematopoietic failures. There are four genes associated with the development of DC: DKC1 gene, which is X-linked, TERC and TERT, which are autosomal dominant, and NOP10, which is autosomal recessive, and the detection of mutations in these genes will be more helpful in the diagnosis of DC. Since leukocyte telomere length test and DC-related gene mutation test are not routinely performed in most units, it is recommended that they be performed at least in patients who have failed immunosuppressive therapy to help clarify the diagnosis and develop a re-treatment plan.