In pediatric AML, UBTF-TDs are associated with distinct genetic features including the frequent co-occurrence of FLT3-internal tandem duplications (FLT3-ITDs) and WT1 mutations, normal karyotype or isolated trisomy 8, mutual exclusivity with known AML subtype-defining lesions (i.e. NPM1 mutations and recurrent fusions) and activation of the HOXA/HOXB cluster genes [13]. This evidence concerns the gene WT1 and acute myeloid leukemia.