Collectively, our and others’ findings, support the notion that deregulated FGFR3-signaling represents an oncogenic driver in NSCLC and a potential mechanism of intrinsic and acquired resistance to EGFR-TKIs that may be reverted by FGFR-TKIs [37,51,68,188,189,190,191]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.