For instance, oncogenic KRAS drives glutamine metabolism in lung adenocarcinoma (Romero et al, 2017), while in lung squamous cell carcinoma, where mTORC1 is frequently hyper‐activated, it has been observed that tumours that are highly resistant to conventional chemotherapy respond to inhibitors targeting the glutamine pathway (Lukey et al, 2018). The gene discussed is KRAS; the disease is lung adenocarcinoma.