In summary, effective metabolic intervention in FLT3-ITD AML necessitates comprehensive evaluation of potential off-target effects in normal proliferative tissues, particularly immune surveillance mechanisms, and implementation of precision medicine approaches incorporating biomarker-driven patient stratification, target-selective inhibition, pharmacokinetically optimized dosing regimens, and synergistic combination therapies that achieve maximal therapeutic efficacy while maintaining acceptable toxicity profiles. This evidence concerns the gene FLT3 and acute myeloid leukemia.