These outcomes identify NF-κB as a major target of CA for its anti-inflammatory and matrix-protective effects in tendinitis, corresponding to previous observations demonstrating that the TNF-β- or TNF-α-promoted activity of NF-κB- and NF-κB-dependent end products is down-regulated by polyphenols in cells of various connective tissues, showing inflammation-protective properties by specifically targeting NF-κB [44,65,66,67,68,69]. This evidence concerns the gene TNF and tendinitis.