STAT1 and acute myeloid leukemia: It has been demonstrated that the autocrine FLT3LG/FLT3 loop promotes proliferation and prevents apoptosis of primary AML blasts and AML cell lines.[56,57] Stimulation of MV4–11 cells with extra FLT3 ligand either by directly adding to the culture medium or by using conditioned medium harvested from MV4–11-R cells can further increase p-STAT1, p-STAT3, p-STAT5, as well as the expression of survivin [50], which correlate with resistance to ABT-869 and other FLT3 inhibitors (AG1296, SU5416 and FLT3 inhibitor III).