PLK1 and neoplasm: This residual cMet/β1‐integrin complex activity, which is dependent upon ligands in the tumor microenvironment, may explain why the combination of PLK1 and cMet inhibition is more effective than single drugs in some mesenchymal NSCLC models and why we observed differences in single‐agent PLK1 inhibitor efficacy in vitro compared with in vivo.