Abnormalities in various subtypes of FGFR may be closely associated with the occurrence and development of tumors. FGFRs are susceptible to various somatic cell alterations, including overexpression, point mutations, and gene translocations, which can lead to carcinogenesis. These mutations are particularly prevalent in solid tumors such as lung cancer, liver cancer, intrahepatic cholangiocarcinoma, breast cancer, gastric cancer, uterine cancer, and bladder cancer, with variations in the types and frequencies of FGFR mutations among different cancer types. Broad-spectrum FGFR inhibitors as well as inhibitors targeting FGFR1-3 have been successfully developed. However, in clinical trials, the three approved FGFR inhibitors still exhibit some treatment-related adverse events (TRAEs), such as hyperphosphatemia, dry mouth, fatigue, skin changes, nail changes, and ocular diseases. The adverse reactions, particularly hyperphosphatemia caused by FGFR1 inhibition, and the issue of resistance have attracted significant attention from researchers. Consequently, several companies are dedicated to developing highly selective inhibitors targeting the precise subtypes of FGFR2, FGFR3, and FGFR4, as well as second-generation FGFR inhibitors aimed at overcoming existing FGFR inhibitor resistance.