Mice constitutively lacking FGFR3 through the germline have skeletal defects but have not been reported to have abnormal cortical morphogenesis. (Colvin et al., 1996; Oh et al., 2003). On the other hand, mice with activating mutations of fgfr3 have an increase in the rate of the cell cycle of cortical stem cells in early neurogenesis and an increase in the generation of TBR2+ IPCs at later stages, leading to increased cortical size and cortical cell number (Inglis-Broadgate et al., 2005; Thomson et al., 2007, 2009). The caudal and lateral areas of the cortex were most affected, reflecting the natural gradient of fgfr3 expression. Thus, FGFR2 and FGFR3 both appear to influence the appropriate proliferation of stem cells in different regions of cortex (anterior and posterior, respectively), suggesting that the regulation of signaling by each of these receptors individually and in combination may be critical for the appropriate expansion of different cortical areas. Compound mutation for fgfr1, fgfr2 and fgfr3 in the early anterior neural tube (driven by foxg1-Cre) results in an almost complete agenesis of both dorsal and ventral telencephalic regions (Gutin et al., 2006; Hebert and Fishell, 2008).