In fact, it seems to be inconsistent with the physiological effects of α2AR as a GPCR; most clinical researchers show that DEX produces anti-inflammatory and organ-protective effects by inhibiting NF-κB. Based on the results of the above discussion, we speculate that DEX may couple with Gs to stimulate AC-cAMP-PKA pathways or affect PI3K/Akt pathways, etc., thus inhibiting NF-κB in situations such as inflammation and ischemia, or applications within a certain concentration range. This evidence concerns the gene NFKB1 and ischemia.