SLC1A5 and hepatocellular carcinoma: These results suggest that the 10–20% residual Na+-dependent glutamine transport activity in HCC ASCT2 knockout cells is not likely entirely attributable to SNAT1/2, a conclusion partially reinforced by lack of measurable upregulation of the SNAT2 System A transporter secondary to shRNA-mediated ASCT2 suppression (Supplemental Figure S14).