As the TRAF6-dependent pathway in IL-17A signaling is NF-κB dependent (47, 48), we sought to elucidate whether IL-17A signaling in frozen shoulder was indeed NF-κB dependent and whether the profibrotic and inflammatory response could be blocked by utilizing a small molecule inhibitor we have previously shown to be effective in a model of tendon disease (49). Here, TRAF6 is linked to disease of the tendon.