The observation that glutamine requirement in cells that escape from TIS is independent from anaplerotic TCA usage also reinforces an important role of ASCT2 as glutamine transporter in these cells, since it has been demonstrated that in cancer cells SNAT1 and SNAT2 mediate net glutamine uptake for glutaminolysis, whereas ASCT2 is required for optimal growth at low glutamine concentrations [52]. Here, SLC1A5 is linked to cancer.