In contrast to the few investigations of EMT as an EGFR TKI acquired resistance mechanism in NSCLC patients, there are some cell studies showing that EGFR TKI treatment could select cells capable of bypassing signaling through activating of RTKs such as IGF1R, FGFR1 or TGFβ and co-occurring induction of EMT could generate mesenchymal-like cells which has survival or anti-apoptotic advantage [29, 30, 33]. This evidence concerns the gene FGFR1 and non-small cell lung carcinoma.