In contrast to the instability of FLT3-ITD during disease evolution,[21] we found that the SF mutation seemed rather stable, analogous to DNMT3A mutations[14, 22] At relapse, the original SF mutations in all seven SF-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. The gene discussed is DNMT3A; the disease is acute myeloid leukemia.