However, several theories have been proposed, including (1) systemic inflammation causing the overexpression of TNF-α and other proinflammatory cytokines (interleukins 6, 1, 17, and 23), which have been reported to be involved in myofibril protein catabolism; (2) local inflammation at the site of attachment of ligaments or tendons to bone (enthesitis) or facet joint arthritis; (3) biomechanical stress; and (4) denervation or/and neuroinflammation of the spinal cord and nerve roots [8, 14, 16, 20–22, 40–43]. This evidence concerns the gene TNF and enthesitis.