Building upon the current demand for safer targeted therapies and emerging evidence of metabolic vulnerabilities in AML, we i) identified the critical binding residues (Phe-236/Lys-179) of fucoxanthin-AKT interaction, and ii) demonstrated the dual mechanism of fucoxanthin, which involves CDK4-mediated cell cycle arrest and GLUT1/ATP metabolic reprogramming. The gene discussed is AKT1; the disease is acute myeloid leukemia.