Interestingly, when we combined the KRAS mutational status with RI, the patients with RAS-high/KRAS wt tumours had the same outcome as those with RAS-high/KRAS mut (Supplementary Fig. 8d), confirming that the tumour progression driven by oncogenic RAS activity is independent of KRAS mutational status. The gene discussed is KRAS; the disease is neoplasm.