The other is that, at least for lung cancers with mutant KRAS, our preclinical data have identified a feasible approach for reactivating the tumor suppressor activity of DLC1 (ref. 4) and suggest that it might be useful to consider combining SRCi with RASi (the AKT inhibitor might not be critical, as the RAS inhibitor would presumably blunt AKT activation). This evidence concerns the gene DLC1 and lung carcinoma.