Over the last decade, major advances in the molecular profiling of acute myeloid leukemia (AML) led to a deeper understanding of its pathobiology and revealed potential therapeutic vulnerabilities. As a result, the classification of AML subtypes has evolved from a morphologic to a molecular and genetic basis. After years of stagnation, we have recently witnessed a rapid expansion of the therapeutic armamentarium for AML. Apart from the use of low-intensity induction therapy with hypomethylating agents and venetoclax in patients who are ineligible for intensive chemotherapy, this includes the introduction of targeted agents for the treatment of AML patients harboring specific driver mutations.
