FGF17 is a secreted fibroblast growth factor that plays a critical role in embryonic brain patterning and development. As a member of the FGF8 subfamily, it functions at the midbrain-hindbrain boundary and regulates neurogenesis through binding to FGF receptors and activation of downstream signaling cascades, including PI3K/AKT and MAPK pathways. The gene is also required for proper ventral body wall closure during embryogenesis 1. Germline FGF17 mutations contribute to congenital hypogonadotropic hypogonadism (CHH) and Kallmann syndrome, accounting for approximately 1.1% of affected individuals 2. Most pathogenic variants impair protein function in vitro 3, and affected patients often carry mutations in related FGF pathway genes. CHH patients with FGF17 mutations respond to hormone replacement therapy with hCG/hMG 4. Recent evidence suggests FGF17 dysregulation contributes to broader neurodevelopmental pathology: reduced FGF17 expression in the BRD2-inhibited forebrain is associated with schizophrenia-like phenotypes in mice, and FGF17 treatment partially rescues developmental deficits in patient-derived organoids 5. FGF17 also holds therapeutic promise in acquired disease contexts. In ischemic stroke, exogenous recombinant FGF17 protects blood-brain barrier integrity through FGFR3-mediated signaling and reduces infarct volume in mice 6. In Parkinson's disease, FGF17-patterned dopaminergic progenitors derived from pluripotent stem cells reverse motor deficits in rodent models 7. Elevated FGF17 expression is associated with poor prognosis in acute myeloid leukemia, suggesting potential utility as a biomarker for patient stratification and response to PI3K/AKT and MAPK pathway inhibitors 8.