Indeed, as hematopoietic cells can acquire somatic mutations in the absence of hematological malignancy (i.e., clonal hematopoiesis of indeterminate potential (CHIP)) and this state of clonal hematopoiesis can be a precursor state of AML, CHIP-associated mutations such as DNMT3A, TET2, and ASXL1 (DTA mutations) often persist at high levels at cytological remission of AML without being associated with any prognostic value or higher risk of relapse [26,66]. This evidence concerns the gene STUB1 and acute myeloid leukemia.