Fgfr2, short for Fibroblast Growth Factor Receptor 2, is a crucial receptor tyrosine kinase. It is involved in various biological processes through activation of fibroblast growth factor signaling pathways, which are essential for cell growth, differentiation, development, and tissue repair [3].

Somatic hotspot mutations, structural amplifications, and fusions of Fgfr2 occur in multiple cancers. Transposon-based screening and tumour modelling in mice identified that truncation of exon 18 of Fgfr2 is a potent driver mutation. Genomic alterations generating stable FGFR2ΔE18 variants are actionable therapeutic targets, confirmed in preclinical mouse and human tumour models, and a clinical trial [3]. In cholangiocarcinoma, FGFR2 fusions, occurring in 10-15% of intrahepatic cholangiocarcinoma patients, have become a promising target for precision oncology. FGFR inhibitors like futibatinib, pemigatinib, and others have shown clinical benefit in patients with FGFR2-altered cholangiocarcinoma, but issues like acquired resistance need further study [1,2,4].

In conclusion, Fgfr2 plays a vital role in cell growth, differentiation, and development through its signaling pathways. The study of Fgfr2 in mouse models has revealed its significance in cancer, especially in cholangiocarcinoma, where FGFR2-targeted therapies are being developed. Understanding Fgfr2's functions and associated mutations provides potential therapeutic strategies for treating related cancers.