Indeed, we found that excessive release of active TGF‐β leads to massive degeneration and apoptosis of tenocytes/TSPCs in the tendon proper as well as chondrogenic lesions during the progression of tendinopathy, consistent with previous findings.[6a] This may be either through a Smad‐dependent mechanism[34] or a JNK pathway.[35]. Here, MAPK8 is linked to disease of the tendon.