Importantly, mutations of DNMT3A, TET2, IDH1/2, or ASXL1 were frequently detected among apparently healthy individuals with clonal hematopoiesis or CHIP (22, 24, 35, 36) and in AML patients who received complete disease remission after chemotherapy (26, 35, 37–39), supporting the pivotal roles of epigenetic deregulation in initiation, clonal evolution and relapse of AMLs. Here, IDH1 is linked to acute myeloid leukemia.