The clinical benefit in terms of improved treatment response and survival with targeted agent use is limited to 47% of patients who harbour an actionable mutation [14], with only 14% of intrahepatic CCA patients possessing an FGFR2 protein alteration [11] and thus eligible for anti-FGFR therapies for intrahepatic CCA. The gene discussed is FGFR2; the disease is cholangiocarcinoma.