We then investigated whether the effects of the various CDC25 inhibitors differed among AML subsets, i.e., patients having AML cells with and without morphological or molecular signs of differentiation (FAB classification, expression of the hematopoietic progenitor cell antigen CD34), or different cytogenetic or molecular genetic abnormalities (Flt3-abnormalities, NPM1 insertions). Here, CD34 is linked to acute myeloid leukemia.