For example, one could speculate that in AML involving translocations in major chromatin remodellers, such as in MLL-AF4 gene fusions, high levels of GFI1 might antagonise runaway activation while the converse would fail to compensate the latter, resulting in additionally impaired differentiation and thus contributing towards more aggressive leukaemogenesis. This evidence concerns the gene AFF1 and acute myeloid leukemia.