Meanwhile, LSCs highly express the fatty acid transporter CD36 and the fatty acid-binding protein 4 (FABP4) that promotes fatty acid uptake and transport to fuel fatty acid lipolysis in bone marrow adipocytes (9–12), Given this evidence, targeting LSC metabolic vulnerabilities like FAM dependency may be a possible approach for eradicating chemoresistant LSCs and improving AML prognosis (13). This evidence concerns the gene FABP4 and acute myeloid leukemia.