CBFB and acute myeloid leukemia: Where, under normal conditions, RUNX1 and CBFB form a heterodimeric protein complex of transcription factors involved in normal myeloid differentiation, in CBF-AML, those fusion transcripts induce, through aberrant epigenetic mechanisms, the silencing of genes involved in normal hematopoiesis[8, 9], and drive the differentiation blockade in CBF-AML[10, 11].