The gene family has three members; , which is a tumor suppressor gene, and and , which are proto-oncogenes. All three genes are known to be expressed in embryonic neural progenitors, and regulates proliferation, neuronal differentiation and migration in the developing neocortex. Here we examined the functions of and in neocortical development. We first attempted, and were unable to generate, E12.5 double mutants, indicating that at least one or gene copy is required for embryonic survival. We therefore focused on single mutants, revealing a telencephalic patterning defect in E12.5 mutants and a proliferation/differentiation defect in mutant neocortices. Specifically, the ventral pallium, a dorsal telencephalic territory, expands into the ventral telencephalon in mutants. In contrast, mutants develop normal regional territories, but neocortical progenitors proliferate less and instead produce more neurons. Finally, in gain-of-function studies, both and reduce neurogenesis and increase BrdU-uptake, indicative of enhanced proliferation, but while effects on proliferation are more immediate, effects are delayed. Taken together, we found that the proto-oncogenes genes are essential regulators of neocortical development and although and functions are similar, they do not entirely overlap. This article has an associated First Person interview with the first author of the paper.