SLC38A7 and acute myeloid leukemia: 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].