Aberrant sensing of nucleic acids originating from the expression of endogenous retroviral elements or accumulating DNA damage and consequent increase in type I IFN levels have been suggested to be a primary driver of pathogenesis of the Aicardi-Goutières Syndrome (AGS), a genetic Leukodystrophy that mainly affects the brain, immune system and skin. Nevertheless, the precise molecular mechanisms triggering the disease remain elusive. On these premises, we arerecruiting a post-doctoral fellow with strong experience in iPSC-based differentiation of Neural Stem Cells and Progenitorand/or innate immunity to viral infectionsto work on a project aimed at evaluating the consequences of the AGS gene defects in the human Central Nervous Systems (CNS) taking advantage of iPSC-based in vitrodifferentiations. The goal is to elucidate the role of different cell types of the CNS, including microglia, in AGSand to investigate what are the endogenous signals that aberrantly activate the disease-causing antiviral responsesin these cells. We combine molecular virology approaches with state-of-the-art NGS technology and proteomics in the highly relevant context of human iPSC-based in vitro disease models.