Moreover, one of the main players in cellular inflammatory processes is the master pro-inflammatory transcription factor, nuclear factor kappa B (NF-κB), which is triggered by different cytokines, such as the tumor necrosis factor (TNF)-α, TNF-β, or interleukin (IL)-1β, and, when activated, leads to further expression and up-regulation of pro-inflammatory genes and catabolic enzymes, contributing to the pathogenesis of tendinitis by further fuelling inflammation and tissue degradation in tendon [10,11,12]. This evidence concerns the gene NFKB1 and tendinitis.