Cerebral cortex development involves a series of neuronal migrations that are regulated through neuronal cell-surface receptors (integrins) interacting with extracellular matrix (ECM) proteins and neighbouring cells (radial glia). Voss and colleagues now report that C3G, a guanine nucleotide exchange factor that can activate, by GTP exchange, signalling from the Ras-like Rap1, acts downstream of neuronal cell-surface receptors to regulate cortical neuron migration in mice (see p. 2139). In C3G-deficient embryos, they report, the cortical preplate does not split into the marginal zone and subplate because of defects in cortical neuron migration. Consequently, the cortical plate does not form, a phenotype that is common to reelin pathway mutants (reelin is an ECM protein that regulates neuronal migration). The attachment of radial glial cells and neurons to the ECM is also disrupted in C3G-deficient embryos, the researchers report. Thus, C3G is essential for two key processes in cortex development -neuronal migration and radial glial attachment - perhaps because reelin and integrin signalling converge at this Ras signalling molecule.