Dysregulation of tyrosine kinases (TKs) may play a role in leukemogenesis by promoting survival and proliferation of acute myeloid leukemia (AML) cells. In AML, the main TKs mutations are produced in Fms-like tyrosine kinase 3 (FLT3), KIT and Janus kinase (JAK) genes, and with less frequency in BCR-ABL. The striking results with TK Inhibitors (TKIs) therapy in BCR-ABL1 chronic myeloid leukemias has paved the way for its clinical development in AML. However, the AML biology complexity seems to prevent TKI therapy from being proposed as a strong shift in the treatment paradigm and prognosis. While some FLT3 inhibitors have shown efficacy in well-designed studies, an increasing number of AML patients are being treated with TKIs as a new standard of care, compassionate use, or in clinical trials. We will review the current clinical evidence concerning the use of TKIs in different subsets of AML (BCR-ABL1, Core Binding Factor, FLT3 mutated, and FLT3 wild-type) to address the main topics concerning these targeted therapies for AML: 1) optimal place (upfront, relapsed/refractory or maintenance); 2) monotherapy or combination; 3) efficacy in TK mutated versus wild-type patients; 4) differences between selective and multi-targeted TKIs. In the next years, clinical trials and real-world data will help answer these questions and establish the impact of TKIs on outcomes of AML patients.

酪氨酸激酶（TKs）的失调可能通过促进急性髓样白血病（AML）细胞的存活和增殖而在白血病发生中发挥作用。在AML中，主要的TKs突变是在Fms样酪氨酸激酶3（FLT3），KIT和Janus激酶（JAK）中产生的基因，在BCR-ABL中的频率较低。TK抑制剂（TKIs）治疗BCR-ABL1慢性粒细胞白血病的惊人结果为AML临床开发铺平了道路。但是，AML生物学的复杂性似乎阻止了TKI治疗被提议为治疗范例和预后的重大转变。尽管某些FLT3抑制剂在经过精心设计的研究中已显示出疗效，但越来越多的AML患者正在接受TKI治疗，作为新的护理标准，富有同情心的使用或临床试验。我们将审查有关在AML的不同子集中使用TKI的当前临床证据（BCR-ABL1，核心结合因子，FLT3突变和FLT3野生型）以解决与这些针对AML的靶向疗法有关的主要主题：1）最佳位置（前期，复发/难治或维持）；2）单一疗法或联合疗法；3）TK突变与野生型患者的疗效；4）选择性和多目标TKI之间的差异。在未来的几年中，临床试验和真实数据将有助于回答这些问题，并确定TKI对AML患者预后的影响。