FGFR2 gene fusions are identified in approximately 10–16% of patients with intrahepatic cholangiocarcinoma and are targets of FGFR tyrosine kinase inhibitors (TKIs). While these agents are clinically effective, nail disorders are a documented class-effect toxicity, occurring in approximately 40%–50% of patients treated with various FGFR inhibitors, often impairing quality of life. We report a case of a 53-year-old man with locally advanced intrahepatic cholangiocarcinoma refractory to standard chemotherapy (cisplatin/gemcitabine, S-1) and proton beam therapy. Comprehensive genomic profiling revealed FGFR2::WAC and KCNH8::FGFR2 fusion genes. Treatment was initiated with pemigatinib (13.5 mg/day). One month later, painful nail deformities appeared, followed by thickening, black discoloration, and brittleness. Despite a dose reduction to 9 mg/day, the nail toxicity remained. Consequently, high-potency topical corticosteroids were administered, and symptoms subsided. After disease progression, the treatment was switched to futibatinib (16 mg daily), and during the three-month administration, the nail disorders did not worsen and tended to improve. In conclusion, we describe a case where severe nail toxicity induced by a reversible FGFR inhibitor was managed by switching to futibatinib and utilizing topical corticosteroids. Although effective treatments for nail-related events are limited, this case suggests the effectiveness of steroid ointments.