Two FGF ligand molecules must bind a receptor dimer in order to cause receptor activation. FGF receptors, akin to other members of the RTK family of proteins, cross-phosphorylate their partner upon ligand binding, triggering the activation of three main intracellular pathways, the Ras/MAP Kinase, PI3 kinase, and PLCγ/Protein Kinase C (Schlessinger, 2000). The cascades eventually impinge upon the transcriptional machinery in the cell nucleus. Although RAS/MAPK and PI3K pathways are known to be important mediators of FGF signaling in the developing CNS, the relative role of each of these signaling pathways and of the other putative nuclear functions of FGF signaling for transcriptional regulation in stem/progenitor cells and biological functions are still unclear.