Our findings support previous studies conducted by Kitai et al. [18] and Manchado et al. [38] demonstrating that in pancreatic and lung cancer cells with mesenchymal phenotypes, inhibition of the MAPK/ERK pathway, downstream of KRAS, results in feedback activation of FGFR1 through downregulation of Sprouty protein expression and resultant activation of pFRS2; the increase in FGFR pathway signaling promotes adaptive resistance. This evidence concerns the gene KRAS and lung cancer.