Acute leukemia often has genetic mutations, what about aplastic anemia? Most scholars used to believe that genetic mutations do not occur in normal people and aplastic anemia, but as research progresses, it is found that healthy normal people also have genetic mutations, and the most common myeloid tumor mutations include DNMT3A, TET2 and ASXL1. The incidence of mutations increases with the age of the patients: it is rare in people under 40 years, very low (1 %) in people under 50 years, and can reach 5 % in people over 60 years and up to 10 % in people over 65-70 years. Two small studies from abroad reported that the incidence of myeloid tumor-associated mutations in aplastic anemia was 5% and 9%, respectively, while two large studies from China and the United Kingdom reported a 17% and 19% incidence; the latter long-term follow-up data showed that the risk of myelodysplastic syndrome/acute myeloid leukemia in patients with aplastic anemia with clonal mutations was much higher than in the non-mutation group (38% versus 5%), with a median time to occur of 7.1 (0.7 to 21.7) years. Subsequently, a multicenter, large-sample, systematic study identified the presence of at least one myeloid neoplasia-associated gene mutation in approximately one-third of patients with aplastic anemia, combining both karyotype and mutation analysis, and 47% of patients with aplastic anemia had clonal hematopoiesis: patients with aplastic anemia with PIGA, BCOR, or BCORL1 mutant clones were strongly The recent outcome and long-term survival were better in patients with aplastic anemia with PIGA, BCOR or BCORL1 mutant clones than in those without mutant clones, while the recent outcome and long-term survival were worst in patients with aplastic anemia with DNMT3A, ASXL1, TP53, RUNX1 or CSMD1 with strong immunosuppression.