In conclusion, our study indicates that MET-mediated activation of Pyk2 could confer resistance to CPL304110, a novel FGFR inhibitor and that the mechanism appears to be common in lung, gastric, and bladder cancer cell lines, thus suggesting that targeting of MET→Pyk2 axis could be a therapeutic strategy to overcome resistance to FGFR inhibitors. Here, MET is linked to urinary bladder cancer.