By using RAGE blocking antibodies, chemical blockers of NF-κB activation and by developing a HSV-derived amplicon vector that induces the expression of a defective RAGE (RAGEΔcyto), we have been able to show that attenuation of the RAGE/NF-κB signaling leads to an improved neuronal survival and to a reduced reactive gliosis after IH exposure. The gene discussed is NFKB1; the disease is isolated hemihyperplasia.