Li et al.18 showed that the clonal patterns with initial mutations (ASXL1, DNMT3A and TET2) promoted the occurrence of MDS, while the some additional driver mutations (SF3B1, U2AF1 or RUNX1) played roles to keep the basic disease features, or give rise to different phenotypes (BCOR, EZH2 or TP53) in individual patients. The gene discussed is TP53; the disease is myelodysplastic syndrome.