Upon RNA virus infection, the signaling adaptor MAVS forms prion-like aggregates to elicit robust antiviral signaling cascades, but excessive MAVS aggregation leads to host immunopathology (e.g., SLE and psoriasis), indicating that it is critical for uncovering the checkpoint that governs the prion-like behavior of MAVS to maintain immune homeostasis. This evidence concerns the gene MAVS and systemic lupus erythematosus.