More recently Ahmad et al. [12] suggested that BCL11B could be a potential oncogene involved in AML with 14q32 aberrations; the identified 4 cases of AML with BCL11B rearrangements (each with a different partner chromosome) expressed both myeloid and T-cell markers and carried AML-associated FLT3 internal tandem duplications (one case also had a FLT-3 D835 mutation). This evidence concerns the gene FLT3 and acute myeloid leukemia.