Given the well-described role of the STING/IRF3 pathway in inflammatory and neurological diseases, we used a rat model of 2VO to assess the hypotheses that STING/TBK1/IRF3 signaling exerts deleterious effects on cerebral hypoperfusion and that RES might suppress the inflammation induced by CCH through dampening the STING/TBK1/IRF3-mediated pathway. Here, TBK1 is linked to columnar cell hyperplasia of the breast.