In addition, treatment of a FLT3-ITD AML cell line and patient sample with the FLT3 inhibitors PKC412 or quizartinib resulted in increased activation of AXL and treatment with PKC412 increased signaling through pathways downstream of AXL, including ERK1/2, AKT, and STAT5 [81]. This evidence concerns the gene AXL and acute myeloid leukemia.