Experiments in mouse models of DS demonstrated that normalization of the IFNR gene copy number can fully or partially rescue several phenotypes in these animals, including impaired fetus growth and neuronal viability (16), as well as lethal antiviral responses, congenital heart malformations, craniofacial anomalies, early developmental delays, and cognitive impairments (17). This evidence concerns the gene IFNAR2 and Dravet syndrome.