FGF-17 is a member of the fibroblast growth factor (FGF) family. The FGF domain of FGF-17 shares significant amino acid sequence similarity with FGF-8 and FGF-18. These three FGFs have distinct and overlapping expression patterns and functions. Like many other FGFs, FGF-17 is a secreted protein and overexpression of FGF-17 in NIH-3T3 cells can induce transformation. Many studies have shown that FGF-17 is involved in the regulation of embryonic brain development. In fact, FGF-17 mRNA can be detected in specific regions of the developing brain, which include the forebrain and the midbrain-hindbrain junction during the early phases of proliferation and neurogenesis. FGF-17-deficient mice have a smaller dorsal frontal cortex, small foliation changes in the cerebellum, and abnormalities in the midbrain-hindbrain region, including the inferior colliculus. FGF-17-deficient mice also showed striking deficiencies in specific social interactions during development and adulthood. It has been shown that FGF-17 can regulate frontal cortex regionalization by coordinating with Emx2 to regulate the expression of Erm, Pea3, and Er81. In addition, FGF-17 can also inhibit oligodendrocyte terminal differentiation via activation of FGFR3 and may also be involved in ovary physiology. FGF-17 mRNA has been detected in oocyte, granulosa, and theca cells. Furthermore, FGF-17 inhibits estradiol and progesterone secretion from granulosa cells and thus may regulate granulosa cell differentiation. FGF-17 has been detected in the walls of all major developing arteries and developing skeletons. FGF-17 was also detected in human prostate cancer and hematopoietic tumors. In vitro studies showed that recombinant FGF-17 can promote proliferation of many prostate cancer cell lines.