Acute myeloid leukemia (AML) is the most common leukemia among adults and has been challenging to treat with modern therapies.1, 2 This disease is highly heterogeneous and characterized by the rapid proliferation of undifferentiated myeloid cells that accumulate within the bone marrow. Several mutations and epigenetic abnormalities characteristic of AML have been targeted through chemotherapies or molecular inhibitors. Fortunately, the relentless pursuit of innovative, effective AML therapies has led to a deeper understanding of AML pathogenesis, such as the role of isocitrate dehydrogenase (IDH) mutations.3 IDH mutations have unique properties that, if properly targeted, may reshape AML patient outcomes and survival rates.
