Regulation, leukemia microenvironment or immune imbal- ance can all cause aml [ 3 ]. fgs-like tyrosine kinase 3 (flt3) is a type iii receptor tyrosine kinase, which is composed of five immunoglobu- lin-like domains in the extracellular region, a paramembrane domain and a tyrosine kinase (tk) domain [ 4 ]. flt3 plays an important role in the survival, proliferation and differen- tiation of hematopoietic cells. flt3 plays an important role in the early stages of both myeloid and lymphoid lineage development and is bound and activated by flt3 ligands. when ftl3 binds to its ligand, it dimerizes and autophos- phorylates to activate tyrosine kinase activity, which in turn activates pi3k/akt and ras/mapk pathways, resulting in dna damage and repair defects, and increases cell prolifer- ation and anti-apoptosis [ 5 ]. clinically, flt3 gene mutation is the most common genetic change and poor prognosis fac- tor in aml patients. flt3 mutation is found in most aml cells, which activates anti-apoptotic and pro-growth signals and stimulates the proliferation of aml cells. internal tan- dem duplication (itd) is the most common type of flt3 mutation (flt3-itd), accounting for about 25% of aml patients. other studies have shown that flt3-itd can acti- vate rho kinase in aml cells, which leads to lim kinase (limk) phosphorylation and affects cytoskeletal dynam- ics, cell growth and apoptosis. other data showed that flt3-itd could promote serine synthesis, and the newly