Abstract: FLT3 internal tandem duplications(FLT3/ITD) is a mutation of juxtamembrane domain of FLT3 gene which lead to a constitutive autophosphorylation and subsequent activation of its downstream effectors, resulting in the inhibition of apoptosis and proliferation advantage of the leukemic clone. From previous clinical studies, it has been regarded as a mutation associated with poor prognosis of acute myeloid leukemia(AML) patients, portends an increased risk of disease relapse following chemotherapy alone.Tyrosine kinase inhibitors(FLT3 inhibitors) have attracted the increased attention of the curative effect for FLT3/ITD positive AML. Currently multi-target tyrosine kinase inhibitor has become a research hotspot in FLT3/ITD positive AML, especially for sorafenib. In this paper, we overview the efficacy and mechanism of sorafenib targeted therapy for FLT3-ITD-positive AML patients.