Clonal hematopoiesis of indeterminate potential (CHIP) serves as a critical precursor to leukemogenesis, characterized by recurrent mutations—most frequently in DNMT3A, TET2, and ASXL1—that emerge in otherwise healthy individuals and significantly elevate the risk of AML and other myeloid neoplasms (9, 10). This evidence concerns the gene TET2 and myeloid neoplasm.