Thus, the preliminary preclinical data presented herein, showing that gilteritinib inhibits AXL at concentrations similar to that for FLT3, suggest that dual inhibition of this pathway may lead to improved efficacy in the treatment of AML; however, it remains unclear whether AXL inhibition played a role in the tumor regression and improved survival induced by gilteritinib in the IBMT model. This evidence concerns the gene FLT3 and acute myeloid leukemia.