During embryonic development, neural stem cells, known as radial glial cells (RGCs), give rise to the different subtypes of excitatory neurons and macroglia cells that form the mature neocortex. Precisely regulated mechanisms are crucial for the proper development of this structure, from the generation of neural cells to their correct migration and establishment of specific connections. Among the many genes described to regulate its proper development, cell-cell adhesion molecules such as Cdh2 or its associated protein Afadin play important roles. Inactivation of these genes in the dorsal telencephalon from early developmental stages results in defects in RGC proliferation and differentiation. The resulting neocortex exhibits notable disorganization and increased progenitor proliferation, leading to an enlargement in its size because of an overproduction of neurons expressing upper-layer neuron markers. Similar alterations have been described in certain murine models of autism spectrum disorder (ASD), as well as in some ASD patients. Interestingly, the behavioral characterization of Afadin cortical conditional mutant mouse revealed important social deficits. In this study, we conducted transcriptomic analysis by RNAseq in these mutant mice at E13.5, revealing differences in neocortical gene expression. Further characterization using RT-qPCR, RNAscope in situ hybridization and immunohistochemistry provided insights into the molecular mechanisms altered following this perturbation. These findings may contribute to reach a better understanding of the underlying mechanisms by which Afadin regulates proper neocortical development.