FGF5 (fibroblast growth factor 5) functions primarily as a negative regulator of the hair growth cycle in mammals. It is expressed in the outer root sheath of hair follicles during the late anagen phase and mediates the transition from the anagen growth phase to the catagen regression phase 1. In humans, inherited FGF5 mutations result in trichomegaly, characterized by abnormally long eyelashes 1. Beyond hair regulation, FGF5 plays roles in broader physiological processes. During embryonic development, it appears as a transient marker of the epiblast-like stage during neural induction from human embryonic stem cells 2. FGF5 also has clinical significance in cardiovascular and kidney diseases. Genetic studies have identified FGF5 as a causal factor in blood pressure regulation and cardiovascular disease risk, with a substantial proportion (30.5%-77.2%) of its effects on coronary artery disease and stroke mediated through blood pressure regulation 3. Large-scale proteomic studies have demonstrated associations between FGF5 levels and incident myocardial infarction, ischemic stroke, and heart failure 4. Additionally, FGF5 variants have been associated with eGFR decline in chr4 kidney disease progression 5. The protein appears to function through growth factor signaling pathways and may represent a promising therapeutic target for multiple conditions.