Clonal hematopoiesis (CH) is an age-related process characterized by mutations in hematopoietic stem/progenitor cells (HSPCs), most commonly in the DNMT3A gene. In CH, mutant HSPCs gain a competitive edge (particularly in the presence of inflammation), which increases the risk of acute myeloid leukemia and other blood disorders. Therefore, understanding the mechanisms that drive this competitive advantage could lead to interventions that mitigate disease risk.

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