Neocortical development starts during embryogenesis with the main neural progenitor cells, classified as apical (APs) and basal progenitors (BPs). BPs are significantly enriched and highly proliferating in gyrencephalic species compared to lissencephalic, leading to neocortical expansion and increased cognitive abilities. BPs’ morphology is highly heterogeneous and correlates with proliferative ability, but the molecular mechanisms that regulate their fate are still unclear. Structural proteins have already been described as determinants of BPs’ morphology and fate; among them, the family of adducins (ADDs) is of particular interest. ADD1, ADD2 and ADD3 anchor the spectrin-actin cytoskeleton to the cell membrane through their interaction with other transmembrane proteins. They have recently been associated with various neurodevelopmental disorders, such as ventriculomegaly and corpus callosum dysgenesis, suggesting a role in the context of neocortical development. Our results show that they are necessary and sufficient for BPs’ abundance, as their overexpression in mouse embryonic neocortex leads to an increase in BPs, while the KO in ferret leads to a reduction in BPs. The increase in BPs in mouse is due to an increase in cell proliferation after ADD1ADD2 OE, while the cell distribution analysis suggests an increase in the delamination after ADD1 OE. Moreover, ADD1ADD2 but not ADD1 alone OE leads to an increase in CTIP2+ neurons, without affecting the SATB2+ subpopulation. Altogether, these results provide further insights into the molecular machinery and mechanisms that regulate BPs’ morphology and functional role in brain development and expansion, but also into the pathological mechanism that underlie certain neurodevelopmental disorders.