Semaphorin 3A (SEMA3A) is a repellent guidance cue considered instrumental in many processes that shape the nervous system during development. It is produced as a secreted protein in mammals and exerts both autocrine and paracrine functions. Interestingly, emerging evidence highlights the association of genetic and functional alterations in SEMA3A or its receptors (NRP1 and PLXNA2) with neurodevelopmental disorders. Indeed, increased SEMA3A expression levels have been detected in the brains of patients with schizophrenia, and several mutations in the SEMA3A, NRP1, or PLXNA2 genes have been described in patients with autism and intellectual disabilities. Therefore, we investigated the growth and differentiation of human neural progenitors (HNPs) following SEMA3A overexpression. To this end, HNPs were transfected with SEMA3A and processed for immunofluorescence for morphological analysis. Our results indicate that increased expression of SEMA3A affects HNPs morphology, inducing axonal retraction and aberrant arborization of apical dendrites. In addition, overexpression of SEMA 3A results in the activation of apoptotic processes, likely affecting neuronal survival. Notably, axonal retraction, dendritic arborization, and neuronal death were prevented when SEMA 3A receptors (NRP1 and PLXNA2) were silenced. In conclusion, our data suggest that SEMA3A plays a critical role during the initial stages of HNPs differentiation, affecting neuronal morphology, connectivity, and survival. Indeed, it is likely that any insult causing SEMA3A overexpression might compromise neuronal homeostasis, making them more vulnerable to other insults during their lifespans. However, how an increase in SEMA3A levels leads to neurodevelopmental disorders needs to be further investigated.