Age-related clonal hematopoiesis is defined as the presence of somatic mutations of genes known to be recurrently mutated in hematologic malignancies in the peripheral blood of healthy individuals.1 When clonal hematopoiesis is associated with a mutation at a variant allele frequency of 0.02 or greater, it is termed “clonal hematopoiesis of indeterminate potential” (CHIP). Classical CHIP genes include epigenetic modifiers such as Dnmt3a, Tet2, and Asxl1, and DNA repair genes such as Tp53 and Ppm1d.2 Although CHIP-associated mutations are most frequent in myeloid neoplasm, some, such as those in Dnmt3a and Tet2, are recurrently observed in lymphoid malignancies as well. Tiacci et al described a case of sequential onset of angioimmunoblastic T-cell lymphoma possessing Tet2 mutations and acute myeloid leukemia within two years in a 45-year-old man.3 This suggested the potential roles of CHIP in the molecular pathogenesis of the sequential/simultaneous onset of two hematologic malignancies, also termed hematological composite malignancies (HCM). However, till now, the association of CHIP mutations with the clone evolution of HCM remains poorly clarified probably due to a low incidence.