Finally, with regards to mechanisms of genetically-driven acquired resistance, gatekeeper mutations that impair drug binding in the ATP-binding pocket of the FGFR kinase domain have been documented in FGFR2 fusion-positive cholangiocarcinoma [105] and FGFR3 fusion-positive urothelial cancer patients treated with FGFR inhibitors [106]. The gene discussed is FGFR2; the disease is cholangiocarcinoma.