Notably, the drug dose of FGFR1 and PLK1 inhibitors used in our in vivo experiments is below the clinically achievable concentrations (Sebastian et al, 2010; Zhang et al, 2012), whereby the synergistic anti‐tumor activity is not compromised by increased side effects, warranting further clinical investigations of FGFR1/PLK1 inhibitor therapy for treating KRAS‐mutant cancers. This evidence concerns the gene PLK1 and cancer.