These findings provide a strong therapeutic rationale to treat epithelial KRAS-mutant lung cancer (high epithelial markers) with clinically available ERBB and MEK inhibitors, and mesenchymal-like KRAS-mutant lung cancers (high FGFR1) by combined therapy with FGFR and MEK inhibitors. This evidence concerns the gene FGFR1 and lung carcinoma.