GATA2 deficiency exacerbates chronic liver injury via disrupting hepatocyte death-regeneration balance: Clinical, histopathological, and molecular evidence

Figure 2 Identification of GATA2 mutation and diagnosis of aplastic anemia in the patient. A: Sanger sequencing of the gene; B: Karyotype analysis; C: Pathological findings of bone marrow biopsy. The proliferation of bone marrow nucleated cells was low; the erythroid lineage was mainly composed of intermediate and late-stage cells; megakaryocytes were rare; lymphocytes were scattered in small numbers; CD34 small vessels (+); few CD61 megakaryocytes (+); D: Flow cytometric analysis. The proportion of CD34+ cells in nuclear cells was about 0.49%, with no obvious abnormality in the immunophenotype. The relative proportion of granulocytes was normal, and the immunophenotypes CD13, CD16, CD15, and CD11b were disordered. Approximately 2.60% of CD19+CD10+ immature B lymphocytes, consistent with normal B progenitor cell proliferation.