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]. The gene discussed is FLT3; the disease is acute myeloid leukemia.