Developmental psychiatric disorders, including schizophrenia, autism, and ADHD, impose significant socio-economic burdens and reduce patients’ life expectancy by 10-20 years due to their early onset and chronic impact. While the genetic implication is evident, pinpointing the implicated risk genes and understanding their mechanisms remains challenging, particularly concerning their influence on brain circuitry formation. Research has spotlighted the 15q13.3 microdeletion in humans as strongly linked to various psychiatric manifestations, with Klf13 gene emerging as a key player in neuronal precursors and differentiation. Our study employs a Klf13+/- mouse model to explore the extent of impairment in normal brain development harbouring this microdeletion. Focusing on two critical cortices, the somatosensory cortex (S1) and prefrontal cortex (PFC), we initially investigated the maturational dynamics of putative GABAergic neurons. Our findings reveal a reduced density of Somatostatin (SST) interneurons in the S1 at postnatal (P) 40 and P60 and in the PFC at P60 in the Klf13+/- mouse model. Conversely, an increased density of Parvalbumin (PV) interneurons was observed in the S1 at P40. These results suggest the vulnerability of medial ganglionic eminence (MGE), where these neurons originate and migrate from. To gain deeper insights, we plan to conduct single-nucleus RNA sequencing on germinal eminences (GEs) at embryonic (E)13.5, elucidating the functional and transcriptional roles of Klf13. Such deep insight to understand the effects of brain circuit perturbations will help to make translational profiles of downstream proteins and identify potential drug targets.