Focal Cortical Dysplasia (FCD) is a developmental malformation of the cerebral cortex and is one of the most common causes of drug-resistant epilepsy in children 0 to 5 years of age, accounting for half of all pediatric epilepsy cases. While effective surgical remedies for pharmacoresistant epilepsy do exist, they are often too expensive and inaccessible to be a viable option for families, highlighting the need for alternative treatment strategies. Previous research has established strong links between FCD, disrupted cortical development, and altered expression of genes regulating neural progenitor proliferation and differentiation, including SOX2, KI67, RBFOX3 (NeuN), and NEUROD1. However, little research has looked at how human-specific regulators of neurodevelopmental signaling pathways may contribute to FCD’s molecular abnormalities. The human-specific gene CHRFAM7A, encoding a dominant-negative modulator of the ⍺7 nicotinic acetylcholine receptor (⍺7-nAChR), has been implicated in inflammation, calcium signaling, neuropsychiatric disorders such as schizophrenia and Alzheimer’s, and human-specific neurodevelopment and cognition. However, it has not been studied in the context of FCD and epilepsy. My study examines the effects of CHRFAM7A knockdown on the expression of SOX2, KI67, RBFOX3, and NEUROD1 using RNA sequencing data derived from human cortical tissue. Observation of a decrease in progenitor-associated markers (SOX2 and KI67), combined with an increase in neuronal differentiation markers (RBFOX3, NEUROD1) would suggest a potential mechanistic link between CHRFAM7A dysregulation and molecular pathways implicated in FCD. These could offer a novel perspective on FCD and pharmacoresistant epilepsy pathogenesis, as well as a foundation for further research on possible non-surgical treatment avenues.