Furthermore, the metabolic adaptability characteristic of AML blasts, including compensatory activation of alternative nutrient scavenging mechanisms (macropinocytosis, upregulation of amino acid transporters such as LAT1/SLC7A5) or metabolic rewiring toward fatty acid β-oxidation, presents significant challenges for durable therapeutic responses to single-agent metabolic inhibitors [154]. The gene discussed is SLC7A5; the disease is acute myeloid leukemia.