Previous research found that in theabsence of Mecp2, NF-kB signaling is increased in the CNS of mice.Genetically attenuating the aberrant NF-kB activation ameliorates several hallmarkphenotypes of RTT, including neuronal morphology, identifying the NF-kB pathway as apotential therapeutic target for RTT. This evidence concerns the gene NFKB1 and Rett syndrome.