Reelin, a large extracellular glycoprotein, binds to the very-low-density lipoprotein andapolipoprotein E receptor 2 receptors, leading to activation of the intracellular adaptor protein Disabled-1 (Dab1). After Dab1 is tyrosine phosphorylated by Src family kinases, the downstream signaling pathway facilitates neuronal migration in the neocortex, cerebellum, and olfactory system. The olfactory epithelium (OE), the peripheral part of the olfactory system, contains olfactory sensory neurons (OSN) that are responsible for detecting odors. Immature OSNs differentiate from multipotent globose basal stem cells and extend their axons toward their synaptic targets within the glomeruli of the olfactory bulb. Previous results from our lab proved that Reelin is expressed by olfactory ensheathing cells (OECs), and that these OECs surround and support the Dab1-expressing axons of the OSNs. This study aims to investigate how the loss of Dab1 affects adult neurogenesis in the OE. Immunohistochemistry was performed on the olfactory epithelium of dab1+/+ and dab1-/- mice to identify cells that express the proliferation marker Ki67, a stem cell marker Sox2, a neuronal precursor marker NeuroD1, and immature GAP43-labeled and adult OMP-labeled OSNs. No differences were detected in the three stem cell populations between dab1+/+ and dab1-/- mice. The average number of GAP43-labeled cells, however, was higher in dab1+/+ compared to dab1-/- mice, although OMP-positive adult OSNs did not differ between genotypes. The width of the OE also did not vary between dab1+/+ and dab1-/- mice. Based on these findings, Dab1 appears to play a role in the development of olfactory progenitors into immature olfactory sensory neurons.