A Nature Communications paper showed that succinate receptor 1 (SUCNR1) functions as a metabolic sentinel that limits blood cell formation and suppresses acute myeloid leukemia progression. The study used genetic and functional assays to connect succinate signaling with stem‑cell fate and leukemogenesis. The work positions SUCNR1 as a novel metabolic checkpoint in hematopoiesis and provides a mechanistic rationale for therapeutic modulation in myeloid malignancies. Hematology drug developers may now assess SUCNR1 as an upstream metabolic target for AML control.