Notably, in the context of mixed cultures of AGS patient iPSC–derived CNS cells, all subsets harbored significant transcriptional alterations, involving not only type I IFN and inflammatory pathways, but also significant upregulation of p53-mediated DNA damage and apoptotic responses as well as metabolic alterations, suggesting that active cross talk between astroglial and neural components contributes to AGS physiopathology. The gene discussed is TP53; the disease is Aicardi-Goutieres syndrome.