Rather AML studies available have indicated that proline uptake is elevated in LSCs isolated from de novo AML patients (165), and that the proline metabolism pathway is significantly impacted by differences in the oncogenic receptor tyrosine kinase FLT3 status of pediatric AML samples (166) or in AML cells overexpressing the proto-oncogene EVI1 (167). The gene discussed is NTRK1; the disease is acute myeloid leukemia.