Alterations to the JAK/STAT3 pathways have been documented in other models of pain in rats (e.g., electroacupuncture and oxaliplatin), where an increase in STAT3 was observed (99–101) or the collagen-induced arthritis in mice in which baicalin, an anti-inflammatory agent, decreased pain as well as concomitant suppression of JAK/STAT3 signaling (102). This evidence concerns the gene STAT3 and arthritic joint disease.