By using NSCLC tumours from genetically engineered mouse models (GEMMs) driven by KrasG12D expression together with loss of Lkb1 (KrasG12D; Lkb1fl/fl, hereafter called KL) or p53 (KrasG12D; p53fl/fl, hereafter called KP), we previously demonstrated that NSCLC histopathologies exhibit differences in oncogenic signalling activities15. The gene discussed is TP53; the disease is neoplasm.