In summary, our data indicate that a series of adaptive changes in cell metabolism arise in response to inhibition of FGFR signaling in FGFR2 fusion+ ICC cells, with alterations in fuel source utilization and mitochondrial dynamics contributing to the maintenance of oxidative phosphorylation (OXPHOS) in the absence of glucose uptake. The gene discussed is FGFR2; the disease is intrahepatic cholangiocarcinoma.