In summary, these findings support a prominent role for the JAK/STAT pathway in the pathogenesis of cPIIRS, support the concept of pathway-instructed therapy to accelerate treatment discovery, and provide a proof of concept for the further study of ruxolitinib as a potential adjuvant therapy of cPIIRS and possibly other types of CNS inflammatory conditions triggered by infections. The gene discussed is SOAT1; the disease is infection.