Detection of viral RNA by cytosolic RIG-I-like receptors (RLRs) induces the production of type I interferons that drive antiviral gene expression and clear infected cells by suppressing cell proliferation and sensitizing cells to apoptosis. Self RNA is modified to avoid recognition by RLRs. When this fails, self RNA is misrecognized as being viral RNA, driving constitutive interferon production in the absence of infection. This causes severe immunopathology, particularly in the brain. We aim to decipher how cytosolic RNA sensing and sterile inflammation are regulated through dynamic post-translational modifications in microglia and other relevant cell types.