The inflammatory effects of IL-1β are well known to be mediated by the MAPK and MYD88/TRAF6/TAK1/IKKl (leading to phosphorylation, ubiquitination, and degradation of IκB-α pathway) signaling cascades, allowing NF-κB translocation to the nucleus, further supporting the key role of this transcription factor as an effective molecular target for the treatment of tendinopathies [20, 21, 110]. Here, NFKB1 is linked to disease of the tendon.