In an independent study, it was shown that the elevated expression of SLC1A5 is driven by the signal transducer and activator of transcription 3 (STAT3)–MYC protooncogene axis in AML stem and progenitor cells (LSCs), enhancing glutamine influx to support the TCA cycle and glutathione production [22]. The gene discussed is SLC1A5; the disease is acute myeloid leukemia.