In the present study, we first reported that dasatinib-induced differentiation of AML cells was accompanied with the activation of the signal transducer and activator of transcription 1 (STAT1), which was evidenced by the augmented phosphorylation of STAT1, the redistribution of STAT1 from cytoplasm to nucleus and the enhanced transcription of STAT1 direct target genes. The gene discussed is STAT1; the disease is acute myeloid leukemia.