TP53 and acute myeloid leukemia: Clonal evolution analysis showed that similar to Patient 1, among all the clones of cells identified in this patient, only the oncogenic clone of cells carrying both TP53 and SF3B1 mutations aggressively and exclusively expanded during disease progression from post-BMT to relapsed-AML, suggesting this clone of cells may be the cause of AML relapse in this patient (Fig. 1D).