In contrast to the instability of FLT3-ITD during disease evolution,34 we found that the TP53 mutation seemed rather stable, analogous to DNMT3A mutations.12 At relapse, the original TP53 mutations in all three TP53-mutated patients studied were retained, but the mutant level in one of them was much reduced at the time of AML relapse, as it could only be detected by a sensitive cloning technique but not by direct sequencing (patient 30, Table 5). This evidence concerns the gene DNMT3A and acute myeloid leukemia.