In the present case, the disappearance of detectable TP53 at relapse despite persistent TET2/DNMT3A mutations suggests that relapse originated from a preleukemic ancestral clone rather than representing continued evolution of the initial TP53-mutant subclone, aligning with established models of AML clonal heterogeneity and evolution (11). This evidence concerns the gene DNMT3A and acute myeloid leukemia.