The robust activation of STAT5 by FLT3-ITD was found to play a role in acquisition of the resistance, because it was reduced by the STAT5 inhibitor pimozide in 32D/ITD cells, MV4–11 cells, or primary AML cells with FLT3-ITD and was acquired through expression of the constitutively activated SATAT5 mutant STAT5A1*6 in 32D/TKD cells (Figs. 2, 3, 6, Supplemental Fig. S1). The gene discussed is STAT5A; the disease is acute myeloid leukemia.