Based on these data, we developed orthogonal approaches that revealed that CBFB::MYH11 is primarily cytoplasmic in primary murine hematopoietic cells and primary human CBFB::MYH11 AML cells, and that the fusion protein sequesters RUNX1 in cytoplasmic aggregates, probably reducing the activity of CBF in the nucleus. This evidence concerns the gene CBFB and acute myeloid leukemia.