Thus, due to these neurodegenerative-mediated changes, it was proposed that the aberrant release of Sema3A from subiculum during early clinical stages of AD resulted in the internalization and transport of Sema3A to CA1, and that this may contribute to the degeneration of neurons in the CA1 field and therefore the decrease of hippocampal functions observed in the disease [123]. The gene discussed is SEMA3A; the disease is Alzheimer disease.