Furthermore, as CCL2-CCR2 signaling has been reported to play a key role in regulating pain in OA,26 we performed IF analysis and quantification and found that the expression of CCL2 was much greater at the endplate area in 5-week-old β-cateninAct mice than in Cre− controls (Fig. S3a, b), suggesting that chondrocyte-derived CCL2 could stimulate excess innervation at the endplate area, contributing to LBP. This evidence concerns the gene CCL2 and Low back pain.