Interestingly, and possibly as a consequence, leukemic cells from both mouse models (GFI136N and GFI1-KD) were more responsive to histone acetyltransferase inhibitors (HATis) than to histone deacetylase inhibitors (HDACis), which are more typically used in experimental therapies for AML (17, 49). This evidence concerns the gene GFI1 and acute myeloid leukemia.