If we consider the secreted signaling molecules expressed by NSCs in the cortical primordium, only disruptions in the FGF pathways have thus far resulted in major defects in cortical development (Hebert et al., 2003; Cheng et al., 2006). Although overexpression of a stabilized β-catenin, which is downstream of the WNT pathway, increases cortical size (Chenn and Walsh, 2002), the disruption of the WNT pathway affects the hippocampus rather than the cortex (Galceran et al., 2000). Thus, normal embryonic cortical development primarily depends on FGF signaling, and in order to better understand the mechanisms mediating these roles, several FGF receptor mutant models have been generated.