Conversely, RAS activation causes resistance to FGFR1 inhibitors in FGFR1-amplified lung cancers [29], suggesting that both FGFR1 and KRAS alterations can sustain aberrant MAPK pathway activation and drive reciprocal resistance to targeted drugs in lung cancer therapy (Figure 3(b)). This evidence concerns the gene FGFR1 and lung carcinoma.