A review report presented that mutation of several transcription factors, including Sox2 gene, results in congenital hypopituitarism or septo-optic dysplasia in murine neonates. Additionally, Pax6 knockdown reduces neurogenic capacity in embryonic stem cells. Constitutive activation of Wnt signaling pathway in forebrain or brainstem precursor cells causes dramatic brain enlargement as well as in the formation of medulloblastoma, a malignant brain tumor in children. Activated Wnt signaling leads to a virtually loss of Pax6 expression, and causes disruption in the proliferation and migration of neurons in mice. Pax6 mutation affects downstream genes on mice cerebellar development for disturbed survival and migration and defects of neurite extension in producing granule cells. Two case reports individually mentioned that mutated Pax6 results in reduced Niraparib vision, photophobia and eyelid ptosis in an autistic child patient, and is responsible for impaired auditory sensory and higher order interhemispheric transfer in a 12 year old child. Above studies indicated that Sox2 and Pax6 are relevant to childhood neurogenesis. In our study, we identified that BPA exposure affects Sox2 and Pax6 prenatally, and this might cause adverse effects on aberrant neuronal or behavioral development for children along with their increasing age. This study found that BPA exposure decreased the gene expression of Sox2 and Pax6 in fetal cord blood, and Sox2 and Pax6 were involved in neuronal development according to network analysis. Findings in this study were consistent with a Xenopus laevis model that prenatal BPA exposure decreases the expression of Sox2 and Pax6 and disrupts Notch signaling to inhibit gamma-secretase activity for neurodegenerative abnormalities. BPA also decreases the expression of Pax6, but not Sox2 to cause malformation of the head region in embryos through estrogen receptor 1 and Notch signaling in Xenopus laevis. Indirect evidence showed that decreased expressions of Sox2 and Pax6 cause adverse effects on neuronal development. Sox2 and Pax6 are lost and undergo glial differentiation after 5-bromo29-deoxyuridine exposure. Conditionally, deleted Sox2 and Pax6 cause proliferative defects, alter morphology and reduce clonogenicity in forebrain-derived neural stem cells. The results of fetal cord blood and network analysis in this study also supported that BPA exposure down-regulated Sox2 and Pax6 expression. The visualized network analysis in response to BPA exposure was addressed in Figure 6 that illustrated that Shh, Notch and VEGFA pathways were in regulation to Sox2 and Pax6 for neuronal signaling including cell differentiation of spinal cord, forebrain neuron differentiation, and regulation of neural precursor cell proliferation. In exposure to BPA, Sox2 and Pax6 were down-regulated by Shh signaling and IGF1 attenuating VEGFA. Pax6 regulates the proliferation of neural progenitor cells in cortical subventricular zone through direct modulation of the Sox2 expression during the late developmental stage in mice.