To target this metabolic fragility unique to the late-stage adenocarcinoma cells, we used 2-deoxy-d-glucose (2-DG) – a glucose analogue and glycolysis inhibitor [[33], [34], [35]] – as a means of preventing compensatory glucose shuttling and further inhibiting tumour cell proliferation mediated by ASNS knockdown (Fig. S5L). The gene discussed is ASNS; the disease is adenocarcinoma.