FLT3 and acute myeloid leukemia: Another possibility is that primary and secondary mutations in FLT3 make the receptor resistant to these inhibitors.14 Earlier studies suggested that acquired mutations in the second part of the kinase domain resulted in a resistant phenotype.15 Expression of several survival genes in resistant cells also led to FLT3 inhibitor resistance.16 Recently, a second-generation FLT3 inhibitor, AC220 (quizartinib), has been used in a phase II clinical trial for patients with relapsed and chemotherapy-refractory AML and induced a composite complete remission rate of 44–54%.