Chemotherapy accelerates CH by selecting stem cells carrying mutations in DDR such as TP53, PPM1D, and CHEK2. 8,9 Similarly, inherited conditions affecting DNA repair, such as in Fanconi anemia (FA), hasten bone marrow failure (BMF) and clonal malignancies by accelerating genomic instability.10 While much research focuses on genetic changes driving clonal dominance, a large percentage of individuals with CH do not harbor any known driver mutations.11–13 This suggests that there must be other yet to be discovered mechanisms by which CH can arise. The gene discussed is PPM1D; the disease is cyclic hematopoiesis.