A functional connection between the MET and FGFR1 pathways is supported by the finding that FGFR inhibitions sensitized MET-amplified gastric cancer cells to treatment with an anti-MET antibody and by the reactivation of MET that drove MAPK activity as a consequence of AR to the FGFR1 inhibitor [30, 31]. The gene discussed is MET; the disease is gastric cancer.