The FGFR (Fibroblast Growth Factor Receptor) signaling pathway plays a crucial role in cellular activities such as proliferation, differentiation, and survival. Dysregulation of this pathway is implicated in numerous human cancers, making FGFR a prominent therapeutic target. This review comprehensively examines the function, signaling pathways, and abnormal alterations of FGFR, its role in tumorigenesis, and the current state of clinical research in FGFR inhibitor therapy. Four FDA-approved drugs—erdaftinib, pemigatinib, infigratinib, and futibatinib—are highlighted, along with their molecular mechanisms and clinical achievements. The review also discusses the challenges of targeting the FGFR pathway, including resistance mechanisms such as gatekeeper mutations, alternative pathways, and potential adverse reactions. Despite these challenges, the potential of FGFR-centric therapies to enhance patient prognosis is underscored, emphasizing the need for continued research to overcome resistance and optimize treatment modalities.The FGFR (Fibroblast Growth Factor Receptor) signaling pathway plays a crucial role in cellular activities such as proliferation, differentiation, and survival. Dysregulation of this pathway is implicated in numerous human cancers, making FGFR a prominent therapeutic target. This review comprehensively examines the function, signaling pathways, and abnormal alterations of FGFR, its role in tumorigenesis, and the current state of clinical research in FGFR inhibitor therapy. Four FDA-approved drugs—erdaftinib, pemigatinib, infigratinib, and futibatinib—are highlighted, along with their molecular mechanisms and clinical achievements. The review also discusses the challenges of targeting the FGFR pathway, including resistance mechanisms such as gatekeeper mutations, alternative pathways, and potential adverse reactions. Despite these challenges, the potential of FGFR-centric therapies to enhance patient prognosis is underscored, emphasizing the need for continued research to overcome resistance and optimize treatment modalities.