Although KP lung mouse tumours are not sensitive to inhibiting glutamine catabolism,88 deleting KEAP1 in these tumours and consequently activating the NRF2 pathway made them heavily reliant on glutamine catabolism,89 supporting both glutathione biosynthesis and the activity of the Krebs cycle.30 In contrast, the presence of activating mutations in CTNNB1 increases the expression of its transcriptional target glutamine synthetase (GS), which leads to increased glutamine production and dependence on mTOR pathway activity, regardless of other co-occurring genetic lesions (e.g. ref. 90). Here, NFE2L2 is linked to neoplasm.